ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Signal Transduction  (348)
  • American Association for the Advancement of Science (AAAS)  (348)
  • EMBO Press
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • 2005-2009  (348)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (348)
  • EMBO Press
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • Nature Publishing Group (NPG)  (63)
Years
Year
  • 1
    facet.materialart.
    Unknown
    Proteins in motion. Introduction (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vinson, Valda J -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):197. doi: 10.1126/science.324.5924.197.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359575" target="_blank"〉PubMed〈/a〉
    Keywords: Evolution, Molecular ; Motion ; Protein Conformation ; Proteins/*chemistry/*physiology ; Signal Transduction ; Thermodynamics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    The Fanconi anemia pathway promotes replication-dependent DNA interstrand cross-link repair (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Fanconi anemia is a human cancer predisposition syndrome caused by mutations in 13 Fanc genes. The disorder is characterized by genomic instability and cellular hypersensitivity to chemicals that generate DNA interstrand cross-links (ICLs). A central event in the activation of the Fanconi anemia pathway is the mono-ubiquitylation of the FANCI-FANCD2 complex, but how this complex confers ICL resistance remains enigmatic. Using a cell-free system, we showed that FANCI-FANCD2 is required for replication-coupled ICL repair in S phase. Removal of FANCD2 from extracts inhibits both nucleolytic incisions near the ICL and translesion DNA synthesis past the lesion. Reversal of these defects requires ubiquitylated FANCI-FANCD2. Our results show that multiple steps of the essential S-phase ICL repair mechanism fail when the Fanconi anemia pathway is compromised.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909596/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909596/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knipscheer, Puck -- Raschle, Markus -- Smogorzewska, Agata -- Enoiu, Milica -- Ho, The Vinh -- Scharer, Orlando D -- Elledge, Stephen J -- Walter, Johannes C -- GM62267/GM/NIGMS NIH HHS/ -- R01 GM062267/GM/NIGMS NIH HHS/ -- R01 GM062267-09/GM/NIGMS NIH HHS/ -- R37 GM044664/GM/NIGMS NIH HHS/ -- R37 GM044664-23/GM/NIGMS NIH HHS/ -- T32CA09216/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1698-701. doi: 10.1126/science.1182372. Epub 2009 Nov 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965384" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell-Free System ; Chromatin/metabolism ; DNA/biosynthesis ; DNA Damage ; *DNA Repair ; *DNA Replication ; Fanconi Anemia/genetics/metabolism ; Fanconi Anemia Complementation Group D2 Protein/*metabolism ; Fanconi Anemia Complementation Group Proteins/*metabolism ; Molecular Sequence Data ; Recombinant Proteins/metabolism ; S Phase ; Signal Transduction ; Ubiquitinated Proteins/metabolism ; Ubiquitination ; Xenopus Proteins/*metabolism ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Function of mitochondrial Stat3 in cellular respiration (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Cytokines such as interleukin-6 induce tyrosine and serine phosphorylation of Stat3 that results in activation of Stat3-responsive genes. We provide evidence that Stat3 is present in the mitochondria of cultured cells and primary tissues, including the liver and heart. In Stat3(-/-) cells, the activities of complexes I and II of the electron transport chain (ETC) were significantly decreased. We identified Stat3 mutants that selectively restored the protein's function as a transcription factor or its functions within the ETC. In mice that do not express Stat3 in the heart, there were also selective defects in the activities of complexes I and II of the ETC. These data indicate that Stat3 is required for optimal function of the ETC, which may allow it to orchestrate responses to cellular homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758306/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758306/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wegrzyn, Joanna -- Potla, Ramesh -- Chwae, Yong-Joon -- Sepuri, Naresh B V -- Zhang, Qifang -- Koeck, Thomas -- Derecka, Marta -- Szczepanek, Karol -- Szelag, Magdalena -- Gornicka, Agnieszka -- Moh, Akira -- Moghaddas, Shadi -- Chen, Qun -- Bobbili, Santha -- Cichy, Joanna -- Dulak, Jozef -- Baker, Darren P -- Wolfman, Alan -- Stuehr, Dennis -- Hassan, Medhat O -- Fu, Xin-Yuan -- Avadhani, Narayan -- Drake, Jennifer I -- Fawcett, Paul -- Lesnefsky, Edward J -- Larner, Andrew C -- CA098924/CA/NCI NIH HHS/ -- P01AG15885/AG/NIA NIH HHS/ -- R01 AI059710/AI/NIAID NIH HHS/ -- R01 AI059710-03/AI/NIAID NIH HHS/ -- R01 AI059710-04/AI/NIAID NIH HHS/ -- R01 CA098924/CA/NCI NIH HHS/ -- R01 CA098924-03/CA/NCI NIH HHS/ -- R01 CA098924-04/CA/NCI NIH HHS/ -- R01 CA098924-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):793-7. doi: 10.1126/science.1164551. Epub 2009 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Respiration ; Cells, Cultured ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Homeostasis ; Mice ; Mitochondria/*metabolism ; Mitochondria, Heart/metabolism ; Mitochondria, Liver/metabolism ; Mitochondrial Membranes/metabolism ; NADH, NADPH Oxidoreductases/metabolism ; Oxidative Phosphorylation ; Phosphorylation ; Precursor Cells, B-Lymphoid/metabolism ; STAT3 Transcription Factor/chemistry/*metabolism ; Serine/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Plant biology. Stressed out over a stress hormone (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2009 May 22;324(5930):1012-3. doi: 10.1126/science.324_1012.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19460982" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*metabolism ; Arabidopsis/genetics/metabolism ; Arabidopsis Proteins/metabolism ; Genes, Plant ; Phosphoprotein Phosphatases/metabolism ; Plant Proteins/*metabolism ; Plants/genetics/*metabolism ; Protein Binding ; Signal Transduction ; Stress, Physiological
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Neuroscience. Went fishing, caught a snake (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meijer, Dies -- New York, N.Y. -- Science. 2009 Sep 11;325(5946):1353-4. doi: 10.1126/science.1180103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Genetics, ErasmusMC, 3000 CA Rotterdam, Netherlands. d.meijer@erasmusmc.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19745142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Homeodomain Proteins/genetics/metabolism ; Myelin Sheath/*physiology ; NF-kappa B/metabolism ; Octamer Transcription Factor-6/genetics/metabolism ; POU Domain Factors/genetics/metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Schwann Cells/*metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Zebrafish/genetics/*metabolism ; Zebrafish Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Innate and adaptive immunity cooperate flexibly to maintain host-microbiota mutualism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: Commensal bacteria in the lower intestine of mammals are 10 times as numerous as the body's cells. We investigated the relative importance of different immune mechanisms in limiting the spread of the intestinal microbiota. Here, we reveal a flexible continuum between innate and adaptive immune function in containing commensal microbes. Mice deficient in critical innate immune functions such as Toll-like receptor signaling or oxidative burst production spontaneously produce high-titer serum antibodies against their commensal microbiota. These antibody responses are functionally essential to maintain host-commensal mutualism in vivo in the face of innate immune deficiency. Spontaneous hyper-activation of adaptive immunity against the intestinal microbiota, secondary to innate immune deficiency, may clarify the underlying mechanisms of inflammatory diseases where immune dysfunction is implicated.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3730530/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3730530/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slack, Emma -- Hapfelmeier, Siegfried -- Stecher, Barbel -- Velykoredko, Yuliya -- Stoel, Maaike -- Lawson, Melissa A E -- Geuking, Markus B -- Beutler, Bruce -- Tedder, Thomas F -- Hardt, Wolf-Dietrich -- Bercik, Premysl -- Verdu, Elena F -- McCoy, Kathy D -- Macpherson, Andrew J -- AI56363/AI/NIAID NIH HHS/ -- CA105001/CA/NCI NIH HHS/ -- R01 CA105001/CA/NCI NIH HHS/ -- U19 AI056363/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):617-20. doi: 10.1126/science.1172747.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON L8S 4L8, Canada. andrew.macpherson@insel.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/biosynthesis/blood/*immunology ; Bacteremia/immunology/microbiology ; Bacteria/growth & development/*immunology/isolation & purification ; Bacterial Infections/immunology/microbiology ; CD4-Positive T-Lymphocytes/immunology ; Colony Count, Microbial ; Enterococcus faecalis/growth & development/immunology/isolation & purification ; Escherichia coli K12/growth & development/immunology/isolation & purification ; Germ-Free Life ; Immunity ; *Immunity, Innate ; Intestinal Mucosa/immunology/*microbiology ; Intestines/immunology/*microbiology ; Lymphoid Tissue/microbiology ; Mice ; Mice, Inbred C57BL ; Permeability ; Respiratory Burst ; Signal Transduction ; Specific Pathogen-Free Organisms ; Spleen/microbiology ; Toll-Like Receptors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    IL-21R on T cells is critical for sustained functionality and control of chronic viral infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Chronic viral infection is often associated with the dysfunction of virus-specific T cells. Our studies using Il21r-deficient (Il21r-/-) mice now suggest that interleukin-21 (IL-21) is critical for the long-term maintenance and functionality of CD8+ T cells and the control of chronic lymphocytic choriomeningitis virus infection in mice. Cell-autonomous IL-21 receptor (IL-21R)-dependent signaling by CD8+ T cells was required for sustained cell proliferation and cytokine production during chronic infection. Il21r-/- mice showed normal CD8+ T cell expansion, effector function, memory homeostasis, and recall responses during acute and after resolved infection with several other nonpersistent viruses. These data suggest that IL-21R signaling is required for the maintenance of polyfunctional T cells during chronic viral infections and have implications for understanding the immune response to other persisting antigens, such as tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frohlich, Anja -- Kisielow, Jan -- Schmitz, Iwana -- Freigang, Stefan -- Shamshiev, Abdijapar T -- Weber, Jacqueline -- Marsland, Benjamin J -- Oxenius, Annette -- Kopf, Manfred -- New York, N.Y. -- Science. 2009 Jun 19;324(5934):1576-80. doi: 10.1126/science.1172815. Epub 2009 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biomedicine, Institute of Integrative Biology, ETH Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Chronic Disease ; Humans ; Immunologic Memory ; Interferon-gamma/biosynthesis ; Lymphocytic Choriomeningitis/*immunology ; Mice ; Mice, Inbred C57BL ; Peptide Fragments/biosynthesis ; Receptors, Interleukin-21/*immunology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Cell biology. Connecting organelles (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wiedemann, Nils -- Meisinger, Chris -- Pfanner, Nikolaus -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):403-4. doi: 10.1126/science.1178016.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Biochemie und Molekularbiologie, Zentrum fur Biochemie und Molekulare Zellforschung and Centre for Biological Signalling Studies, Universitat Freiburg, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628848" target="_blank"〉PubMed〈/a〉
    Keywords: Endoplasmic Reticulum/*physiology/ultrastructure ; Membrane Proteins/genetics/*physiology ; Mitochondria/*physiology/ultrastructure ; Mitochondrial Proteins/genetics/*physiology ; Signal Transduction ; Yeasts
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    A frazzled/DCC-dependent transcriptional switch regulates midline axon guidance (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: Precise wiring of the nervous system depends on coordinating the action of conserved families of proteins that direct axons to their appropriate targets. Slit-roundabout repulsion and netrin-deleted in colorectal cancer (DCC) (frazzled) attraction must be tightly regulated to control midline axon guidance in vertebrates and invertebrates, but the mechanism mediating this regulation is poorly defined. Here, we show that the Fra receptor has two genetically separable functions in regulating midline guidance in Drosophila. First, Fra mediates canonical chemoattraction in response to netrin, and, second, it functions independently of netrin to activate commissureless transcription, allowing attraction to be coupled to the down-regulation of repulsion in precrossing commissural axons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078765/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Long -- Garbe, David S -- Bashaw, Greg J -- NS046333/NS/NINDS NIH HHS/ -- NS054739/NS/NINDS NIH HHS/ -- R01 NS046333/NS/NINDS NIH HHS/ -- R01 NS046333-07/NS/NINDS NIH HHS/ -- R01 NS054739/NS/NINDS NIH HHS/ -- R01 NS054739-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):944-7. doi: 10.1126/science.1171320. Epub 2009 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Pennsylvania School of Medicine, 1113 BRB2/3, 421 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; *Gene Expression Regulation, Developmental ; Membrane Proteins/*genetics/metabolism ; Mutation ; Nerve Growth Factors/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Nervous System/embryology/growth & development ; Neurons/*physiology ; RNA, Messenger/genetics/metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, Immunologic/genetics ; Signal Transduction ; Transcription, Genetic ; *Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Effects of genetic perturbation on seasonal life history plasticity (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-20
    Description: Like many species, the model plant Arabidopsis thaliana exhibits multiple different life histories in natural environments. We grew mutants impaired in different signaling pathways in field experiments across the species' native European range in order to dissect the mechanisms underlying this variation. Unexpectedly, mutational loss at loci implicated in the cold requirement for flowering had little effect on life history except in late-summer cohorts. A genetically informed photothermal model of progression toward flowering explained most of the observed variation and predicted an abrupt transition from autumn flowering to spring flowering in late-summer germinants. Environmental signals control the timing of this transition, creating a critical window of acute sensitivity to genetic and climatic change that may be common for seasonally regulated life history traits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilczek, Amity M -- Roe, Judith L -- Knapp, Mary C -- Cooper, Martha D -- Lopez-Gallego, Cristina -- Martin, Laura J -- Muir, Christopher D -- Sim, Sheina -- Walker, Alexis -- Anderson, Jillian -- Egan, J Franklin -- Moyers, Brook T -- Petipas, Renee -- Giakountis, Antonis -- Charbit, Erika -- Coupland, George -- Welch, Stephen M -- Schmitt, Johanna -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):930-4. doi: 10.1126/science.1165826. Epub 2009 Jan 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Brown University, Providence, RI 02912, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19150810" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Arabidopsis/*genetics/*growth & development ; Environment ; Flowers/growth & development ; Mutation ; Photoperiod ; Seasons ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 11
    facet.materialart.
    Unknown
    CD24 and Siglec-10 selectively repress tissue damage-induced immune responses (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-07
    Description: Patten recognition receptors, which recognize pathogens or components of injured cells (danger), trigger activation of the innate immune system. Whether and how the host distinguishes between danger- versus pathogen-associated molecular patterns remains unresolved. We report that CD24-deficient mice exhibit increased susceptibility to danger- but not pathogen-associated molecular patterns. CD24 associates with high mobility group box 1, heat shock protein 70, and heat shock protein 90; negatively regulates their stimulatory activity; and inhibits nuclear factor kappaB (NF-kappaB) activation. This occurs at least in part through CD24 association with Siglec-10 in humans or Siglec-G in mice. Our results reveal that the CD24-Siglec G pathway protects the host against a lethal response to pathological cell death and discriminates danger- versus pathogen-associated molecular patterns.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765686/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765686/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Guo-Yun -- Tang, Jie -- Zheng, Pan -- Liu, Yang -- AI064350/AI/NIAID NIH HHS/ -- CA112001/CA/NCI NIH HHS/ -- CA58033/CA/NCI NIH HHS/ -- R01 AI064350/AI/NIAID NIH HHS/ -- R01 AI064350-04/AI/NIAID NIH HHS/ -- R01 CA058033/CA/NCI NIH HHS/ -- R01 CA058033-16A2/CA/NCI NIH HHS/ -- R01 CA112001/CA/NCI NIH HHS/ -- R01 CA112001-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1722-5. doi: 10.1126/science.1168988. Epub 2009 Mar 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunotherapy, Department of Surgery, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19264983" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaminophen/toxicity ; Animals ; Antigens, CD24/genetics/*metabolism ; Cytokines/metabolism ; Dendritic Cells/immunology ; HMGB1 Protein/chemistry/immunology/*metabolism ; HSP70 Heat-Shock Proteins/metabolism ; HSP90 Heat-Shock Proteins/metabolism ; Humans ; *Immunity, Innate ; Immunoprecipitation ; Inflammation/*immunology ; Lectins/*metabolism ; Lipopolysaccharides/toxicity ; Liver/immunology/pathology ; Mice ; Mutant Proteins/chemistry/metabolism ; Necrosis/chemically induced/immunology ; Protein Structure, Tertiary ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism ; Receptors, Antigen, B-Cell/*metabolism ; Receptors, Cell Surface/metabolism ; Receptors, Pattern Recognition/immunology/metabolism ; Signal Transduction ; Transcription Factor RelA/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 12
    facet.materialart.
    Unknown
    Smoothened mutation confers resistance to a Hedgehog pathway inhibitor in medulloblastoma (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-04
    Description: The Hedgehog (Hh) signaling pathway is inappropriately activated in certain human cancers, including medulloblastoma, an aggressive brain tumor. GDC-0449, a drug that inhibits Hh signaling by targeting the serpentine receptor Smoothened (SMO), has produced promising anti-tumor responses in early clinical studies of cancers driven by mutations in this pathway. To evaluate the mechanism of resistance in a medulloblastoma patient who had relapsed after an initial response to GDC-0449, we determined the mutational status of Hh signaling genes in the tumor after disease progression. We identified an amino acid substitution at a conserved aspartic acid residue of SMO that had no effect on Hh signaling but disrupted the ability of GDC-0449 to bind SMO and suppress this pathway. A mutation altering the same amino acid also arose in a GDC-0449-resistant mouse model of medulloblastoma. These findings show that acquired mutations in a serpentine receptor with features of a G protein-coupled receptor can serve as a mechanism of drug resistance in human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yauch, Robert L -- Dijkgraaf, Gerrit J P -- Alicke, Bruno -- Januario, Thomas -- Ahn, Christina P -- Holcomb, Thomas -- Pujara, Kanan -- Stinson, Jeremy -- Callahan, Christopher A -- Tang, Tracy -- Bazan, J Fernando -- Kan, Zhengyan -- Seshagiri, Somasekar -- Hann, Christine L -- Gould, Stephen E -- Low, Jennifer A -- Rudin, Charles M -- de Sauvage, Frederic J -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):572-4. doi: 10.1126/science.1179386. Epub 2009 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19726788" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Anilides/metabolism/pharmacology/*therapeutic use ; Animals ; Antineoplastic Agents/metabolism/pharmacology/*therapeutic use ; Brain Neoplasms/*drug therapy/*genetics/pathology ; Cell Line, Tumor ; Cinnamates/pharmacology ; Drug Resistance, Neoplasm ; Hedgehog Proteins/antagonists & inhibitors/genetics/*metabolism ; Humans ; Medulloblastoma/*drug therapy/*genetics/pathology ; Mice ; Molecular Sequence Data ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Mutation, Missense ; Neoplasm Metastasis ; Protein Conformation ; Pyridines/metabolism/pharmacology/*therapeutic use ; Receptors, Cell Surface/genetics/metabolism ; Receptors, G-Protein-Coupled/antagonists & ; inhibitors/chemistry/*genetics/metabolism ; Signal Transduction ; Veratrum Alkaloids/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 13
    facet.materialart.
    Unknown
    Impact of genome reduction on bacterial metabolism and its regulation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: To understand basic principles of bacterial metabolism organization and regulation, but also the impact of genome size, we systematically studied one of the smallest bacteria, Mycoplasma pneumoniae. A manually curated metabolic network of 189 reactions catalyzed by 129 enzymes allowed the design of a defined, minimal medium with 19 essential nutrients. More than 1300 growth curves were recorded in the presence of various nutrient concentrations. Measurements of biomass indicators, metabolites, and 13C-glucose experiments provided information on directionality, fluxes, and energetics; integration with transcription profiling enabled the global analysis of metabolic regulation. Compared with more complex bacteria, the M. pneumoniae metabolic network has a more linear topology and contains a higher fraction of multifunctional enzymes; general features such as metabolite concentrations, cellular energetics, adaptability, and global gene expression responses are similar, however.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yus, Eva -- Maier, Tobias -- Michalodimitrakis, Konstantinos -- van Noort, Vera -- Yamada, Takuji -- Chen, Wei-Hua -- Wodke, Judith A H -- Guell, Marc -- Martinez, Sira -- Bourgeois, Ronan -- Kuhner, Sebastian -- Raineri, Emanuele -- Letunic, Ivica -- Kalinina, Olga V -- Rode, Michaela -- Herrmann, Richard -- Gutierrez-Gallego, Ricardo -- Russell, Robert B -- Gavin, Anne-Claude -- Bork, Peer -- Serrano, Luis -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1263-8. doi: 10.1126/science.1177263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Genomic Regulation (CRG) and Universitat Pompeu Fabra, Avenida Dr. Aiguader 88, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965476" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Bacterial Proteins/*metabolism ; Culture Media ; Energy Metabolism ; Enzymes/genetics/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Bacterial ; *Genome, Bacterial ; Glycolysis ; *Metabolic Networks and Pathways ; Mycoplasma pneumoniae/*genetics/growth & development/*metabolism ; RNA, Bacterial/genetics/metabolism ; Signal Transduction ; Systems Biology ; Transcription, Genetic ; rRNA Operon
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 14
    facet.materialart.
    Unknown
    Small-molecule activators of a proenzyme (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-07
    Description: Virtually all of the 560 human proteases are stored as inactive proenyzmes and are strictly regulated. We report the identification and characterization of the first small molecules that directly activate proenzymes, the apoptotic procaspases-3 and -6. It is surprising that these compounds induce autoproteolytic activation by stabilizing a conformation that is both more active and more susceptible to intermolecular proteolysis. These procaspase activators bypass the normal upstream proapoptotic signaling cascades and induce rapid apoptosis in a variety of cell lines. Systematic biochemical and biophysical analyses identified a cluster of mutations in procaspase-3 that resist small-molecule activation both in vitro and in cells. Compounds that induce gain of function are rare, and the activators reported here will enable direct control of the executioner caspases in apoptosis and in cellular differentiation. More generally, these studies presage the discovery of other proenzyme activators to explore fundamental processes of proenzyme activation and their fate-determining roles in biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886848/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886848/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolan, Dennis W -- Zorn, Julie A -- Gray, Daniel C -- Wells, James A -- F32 CA119641/CA/NCI NIH HHS/ -- F32 CA119641-03/CA/NCI NIH HHS/ -- R01 CA136779/CA/NCI NIH HHS/ -- R21 N5057022/PHS HHS/ -- New York, N.Y. -- Science. 2009 Nov 6;326(5954):853-8. doi: 10.1126/science.1177585.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmaceutical Chemistry, University of California, San Francisco, Byers Hall, 1700 4th Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Benzopyrans/chemistry/*metabolism/pharmacology ; Biocatalysis ; Caspase 3/chemistry/genetics/*metabolism ; Caspase 6/chemistry/genetics/*metabolism ; Caspase Inhibitors ; Catalytic Domain ; Cell Line, Transformed ; Cell Line, Tumor ; Cells, Cultured ; Enzyme Activation ; Enzyme Activators/chemistry/*metabolism/pharmacology ; Enzyme Inhibitors/metabolism/pharmacology ; Enzyme Precursors/antagonists & inhibitors/chemistry/genetics/*metabolism ; Granzymes/metabolism ; Humans ; Imidazoles/chemistry/*metabolism/pharmacology ; Kinetics ; Mice ; Molecular Structure ; Mutagenesis ; Pyridines/chemistry/*metabolism/pharmacology ; Signal Transduction ; Small Molecule Libraries/chemistry/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 15
    facet.materialart.
    Unknown
    Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of T follicular helper cell differentiation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-18
    Description: Effective B cell-mediated immunity and antibody responses often require help from CD4+ T cells. It is thought that a distinct CD4+ effector T cell subset, called T follicular helper cells (T(FH)), provides this help; however, the molecular requirements for T(FH) differentiation are unknown. We found that expression of the transcription factor Bcl6 in CD4+ T cells is both necessary and sufficient for in vivo T(FH) differentiation and T cell help to B cells in mice. In contrast, the transcription factor Blimp-1, an antagonist of Bcl6, inhibits T(FH) differentiation and help, thereby preventing B cell germinal center and antibody responses. These findings demonstrate that T(FH) cells are required for proper B cell responses in vivo and that Bcl6 and Blimp-1 play central but opposing roles in T(FH) differentiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2766560/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2766560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnston, Robert J -- Poholek, Amanda C -- DiToro, Daniel -- Yusuf, Isharat -- Eto, Danelle -- Barnett, Burton -- Dent, Alexander L -- Craft, Joe -- Crotty, Shane -- AR40072/AR/NIAMS NIH HHS/ -- AR44076/AR/NIAMS NIH HHS/ -- P30 AR053495/AR/NIAMS NIH HHS/ -- R01 063107/PHS HHS/ -- R01 072543/PHS HHS/ -- R01 AI063107/AI/NIAID NIH HHS/ -- R01 AI063107-01A1/AI/NIAID NIH HHS/ -- R01 AI072543/AI/NIAID NIH HHS/ -- R01 AI072543-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 21;325(5943):1006-10. doi: 10.1126/science.1175870. Epub 2009 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Vaccine Discovery, La Jolla Institute for Allergy and Immunology (LIAI), 9420 Athena Circle, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19608860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; Arenaviridae Infections/immunology ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/cytology/immunology ; Cell Differentiation ; Cell Lineage ; Cytokines/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation ; Germinal Center/cytology/immunology ; Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 16
    facet.materialart.
    Unknown
    The aryl hydrocarbon nuclear translocator alters CD30-mediated NF-kappaB-dependent transcription (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Expression and signaling of CD30, a tumor necrosis factor receptor family member, is up-regulated in numerous lymphoid-derived neoplasias, most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymphoma. To gain insight into the mechanism of CD30 signaling, we used an affinity purification strategy that led to the identification of the aryl hydrocarbon receptor nuclear translocator (ARNT) as a CD30-interacting protein that modulated the activity of the RelB subunit of the transcription factor nuclear factor kappaB (NF-kappaB). ALCL cells that were deficient in ARNT exhibited defects in RelB recruitment to NF-kappaB-responsive promoters, whereas RelA recruitment to the same sites was potentiated, resulting in the augmented expression of these NF-kappaB-responsive genes. These findings indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682336/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682336/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, Casey W -- Duckett, Colin S -- R01 GM067827/GM/NIGMS NIH HHS/ -- R01 GM067827-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):251-5. doi: 10.1126/science.1162818.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131627" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD30/*metabolism ; Aryl Hydrocarbon Receptor Nuclear Translocator/chemistry/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; DNA/metabolism ; Feedback, Physiological ; Gene Expression Regulation ; Humans ; Lymphoma, Large-Cell, Anaplastic/genetics/metabolism ; Molecular Sequence Data ; NF-kappa B/genetics/metabolism ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Tumor Necrosis Factor, Type II/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factor RelB/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 17
    facet.materialart.
    Unknown
    Priming in systemic plant immunity (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Plants possess inducible systemic defense responses when locally infected by pathogens. Bacterial infection results in the increased accumulation of the mobile metabolite azelaic acid, a nine-carbon dicarboxylic acid, in the vascular sap of Arabidopsis that confers local and systemic resistance against the pathogen Pseudomonas syringae. Azelaic acid primes plants to accumulate salicylic acid (SA), a known defense signal, upon infection. Mutation of the AZELAIC ACID INDUCED 1 (AZI1) gene, which is induced by azelaic acid, results in the specific loss of systemic immunity triggered by pathogen or azelaic acid and of the priming of SA induction in plants. Furthermore, the predicted secreted protein AZI1 is also important for generating vascular sap that confers disease resistance. Thus, azelaic acid and AZI1 are components of plant systemic immunity involved in priming defenses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jung, Ho Won -- Tschaplinski, Timothy J -- Wang, Lin -- Glazebrook, Jane -- Greenberg, Jean T -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):89-91. doi: 10.1126/science.1170025.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Cell Biology, University of Chicago, 1103 East 57th Street EBC410, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342588" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*immunology/metabolism/*microbiology ; Arabidopsis Proteins/*genetics/physiology ; Dicarboxylic Acids/*metabolism/pharmacology ; Gene Expression Regulation, Plant ; *Genes, Plant ; Immunity, Innate ; Mutation ; Oligonucleotide Array Sequence Analysis ; Plant Diseases/*immunology ; Plant Leaves/immunology/metabolism ; Pseudomonas syringae/growth & development/*immunology/pathogenicity ; Salicylic Acid/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 18
    facet.materialart.
    Unknown
    The extracellular matrix: not just pretty fibrils (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: The extracellular matrix (ECM) and ECM proteins are important in phenomena as diverse as developmental patterning, stem cell niches, cancer, and genetic diseases. The ECM has many effects beyond providing structural support. ECM proteins typically include multiple, independently folded domains whose sequences and arrangement are highly conserved. Some of these domains bind adhesion receptors such as integrins that mediate cell-matrix adhesion and also transduce signals into cells. However, ECM proteins also bind soluble growth factors and regulate their distribution, activation, and presentation to cells. As organized, solid-phase ligands, ECM proteins can integrate complex, multivalent signals to cells in a spatially patterned and regulated fashion. These properties need to be incorporated into considerations of the functions of the ECM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536535/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536535/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hynes, Richard O -- P01 HL066105/HL/NHLBI NIH HHS/ -- R01 CA017007/CA/NCI NIH HHS/ -- U54 CA126515/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1216-9. doi: 10.1126/science.1176009.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. rohynes@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; *Cell Physiological Processes ; Extracellular Matrix/*physiology ; Extracellular Matrix Proteins/chemistry/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Models, Biological ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Signal Transduction ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 19
    facet.materialart.
    Unknown
    Pre-target axon sorting establishes the neural map topography (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: Sensory information detected by the peripheral nervous system is represented as a topographic map in the brain. It has long been thought that the topography of the map is determined by graded positional cues that are expressed by the target. Here, we analyzed the pre-target axon sorting for olfactory map formation in mice. In olfactory sensory neurons, an axon guidance receptor, Neuropilin-1, and its repulsive ligand, Semaphorin-3A, are expressed in a complementary manner. We found that expression levels of Neuropilin-1 determined both pre-target sorting and projection sites of axons. Olfactory sensory neuron-specific knockout of Semaphorin-3A perturbed axon sorting and altered the olfactory map topography. Thus, pre-target axon sorting plays an important role in establishing the topographic order based on the relative levels of guidance molecules expressed by axons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Takeshi -- Yamazaki, Takahiro -- Kobayakawa, Reiko -- Kobayakawa, Ko -- Abe, Takaya -- Suzuki, Misao -- Sakano, Hitoshi -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):585-90. doi: 10.1126/science.1173596. Epub 2009 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19589963" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Brain Mapping ; Cell Communication ; Cues ; Cyclic AMP/metabolism ; Ligands ; Mice ; Mice, Knockout ; Mice, Transgenic ; Neuroglia/physiology ; Neuropilin-1/*metabolism ; Olfactory Bulb/cytology/*physiology ; Olfactory Mucosa/cytology/physiology ; Olfactory Pathways/cytology/*physiology ; Olfactory Receptor Neurons/cytology/*physiology ; Receptors, Odorant/metabolism ; Semaphorin-3A/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 20
    facet.materialart.
    Unknown
    The optogenetic catechism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: An emerging set of methods enables an experimental dialogue with biological systems composed of many interacting cell types--in particular, with neural circuits in the brain. These methods are sometimes called "optogenetic" because they use light-responsive proteins ("opto-") encoded in DNA ("-genetic"). Optogenetic devices can be introduced into tissues or whole organisms by genetic manipulation and be expressed in anatomically or functionally defined groups of cells. Two kinds of devices perform complementary functions: Light-driven actuators control electrochemical signals, while light-emitting sensors report them. Actuators pose questions by delivering targeted perturbations; sensors (and other measurements) signal answers. These catechisms are beginning to yield previously unattainable insight into the organization of neural circuits, the regulation of their collective dynamics, and the causal relationships between cellular activity patterns and behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miesenbock, Gero -- G0700888/Medical Research Council/United Kingdom -- G0701225/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):395-9. doi: 10.1126/science.1174520.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK. gero.miesenboeck@dpag.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833960" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology/instrumentation/*methods ; Brain/*physiology ; Calcium/metabolism ; Gene Expression Profiling ; *Genetic Engineering ; *Light ; Membrane Potentials ; Neural Pathways/physiology ; Neurons/*physiology ; Neurosciences/*methods ; Photons ; Proteins/*metabolism ; Signal Transduction ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 21
    facet.materialart.
    Unknown
    The insect neuropeptide PTTH activates receptor tyrosine kinase torso to initiate metamorphosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived prothoracicotropic hormone (PTTH), which stimulates the production of the molting hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rewitz, Kim F -- Yamanaka, Naoki -- Gilbert, Lawrence I -- O'Connor, Michael B -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1403-5. doi: 10.1126/science.1176450.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965758" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bombyx/*genetics/metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/embryology/genetics/*growth & development/metabolism ; Embryo, Nonmammalian/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Insect Hormones/chemistry/*metabolism ; Larva/growth & development ; Ligands ; *Metamorphosis, Biological ; Molecular Sequence Data ; Neurons/metabolism ; Phosphorylation ; Pupa/growth & development ; RNA Interference ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 22
    facet.materialart.
    Unknown
    Mechanically activated integrin switch controls alpha5beta1 function (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: The cytoskeleton, integrin-mediated adhesion, and substrate stiffness control a common set of cell functions required for development and homeostasis that are often deranged in cancer. The connection between these mechanical elements and chemical signaling processes is not known. Here, we show that alpha(5)beta(1) integrin switches between relaxed and tensioned states in response to myosin II-generated cytoskeletal force. Force combines with extracellular matrix stiffness to generate tension that triggers the integrin switch. This switch directly controls the alpha(5)beta(1)-fibronectin bond strength through engaging the synergy site in fibronectin and is required to generate signals through phosphorylation of focal adhesion kinase. In the context of tissues, this integrin switch connects cytoskeleton and extracellular matrix mechanics to adhesion-dependent motility and signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedland, Julie C -- Lee, Mark H -- Boettiger, David -- GM57388/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):642-4. doi: 10.1126/science.1168441.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179533" target="_blank"〉PubMed〈/a〉
    Keywords: Actins ; Biophysical Phenomena ; Cell Adhesion ; Cell Line, Tumor ; Cytoskeleton/*physiology ; Fibronectins/chemistry/*metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Humans ; Integrin alpha5beta1/*chemistry/*metabolism ; Ligands ; Models, Molecular ; Myosin Type II/antagonists & inhibitors/metabolism ; Phosphorylation ; Protein Binding ; Protein Conformation ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 23
    facet.materialart.
    Unknown
    Systems biology. Attractors and democratic dynamics (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bar-Yam, Yaneer -- Harmon, Dion -- de Bivort, Benjamin -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1016-7. doi: 10.1126/science.1163225.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New England Complex Systems Institute, 24 Mt. Auburn Street, Cambridge, MA 02138, USA. yaneer@necsi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19229023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Profiling ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Models, Genetic ; Phenotype ; Signal Transduction ; Systems Biology ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 24
    facet.materialart.
    Unknown
    The tail of integrins, talin, and kindlins (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: Integrins are transmembrane cell-adhesion molecules that carry signals from the outside to the inside of the cell and vice versa. Like other cell surface receptors, integrins signal in response to ligand binding; however, events within the cell can also regulate the affinity of integrins for ligands. This feature is important in physiological situations such as those in blood, in which cells are always in close proximity to their ligands, yet cell-ligand interactions occur only after integrin activation in response to specific external cues. This review focuses on the mechanisms whereby two key proteins, talin and the kindlins, regulate integrin activation by binding the tails of integrin-beta subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moser, Markus -- Legate, Kyle R -- Zent, Roy -- Fassler, Reinhard -- DK 69921/DK/NIDDK NIH HHS/ -- DK075594/DK/NIDDK NIH HHS/ -- DK65138/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):895-9. doi: 10.1126/science.1163865.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Humans ; Integrins/chemistry/*metabolism ; Ligands ; Membrane Proteins/chemistry/*metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Signal Transduction ; Talin/chemistry/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 25
    facet.materialart.
    Unknown
    To nibble at plant resistance proteins (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-09
    Description: To intercept invading microbes that threaten growth and reproduction, plants evolved a sophisticated innate immune system. Recognition of specialized pathogens is mediated by resistance proteins that function as molecular switches. Pathogen perception by these multidomain proteins seems to trigger a series of conformational changes dependent on nucleotide exchange. The activated resistance protein switches on host defenses, often culminating in the death of infected cells. Given their control over life and death, activity of these proteins requires tight regulation that involves intramolecular interactions between the various domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takken, F L W -- Tameling, W I L -- New York, N.Y. -- Science. 2009 May 8;324(5928):744-6. doi: 10.1126/science.1171666.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Pathology, Swammerdam Institute for Life Sciences (SILS), University of Amsterdam, Post Office Box 94215, 1090 GE Amsterdam, the Netherlands. F.L.W.Takken@uva.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423813" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/metabolism ; Adenosine Triphosphatases/chemistry/genetics/*metabolism ; Adenosine Triphosphate/metabolism ; Host-Pathogen Interactions ; Immunity, Innate ; Plant Diseases/*immunology ; Plant Proteins/chemistry/genetics/*metabolism ; Plants/*immunology/metabolism/*microbiology ; Protein Conformation ; Protein Multimerization ; Protein Structure, Tertiary ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 26
    facet.materialart.
    Unknown
    Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-26
    Description: Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease. The factors regulating this process are only partly understood. Abeta aggregation is a concentration-dependent process that is likely responsive to changes in brain interstitial fluid (ISF) levels of Abeta. Using in vivo microdialysis in mice, we found that the amount of ISF Abeta correlated with wakefulness. The amount of ISF Abeta also significantly increased during acute sleep deprivation and during orexin infusion, but decreased with infusion of a dual orexin receptor antagonist. Chronic sleep restriction significantly increased, and a dual orexin receptor antagonist decreased, Abeta plaque formation in amyloid precursor protein transgenic mice. Thus, the sleep-wake cycle and orexin may play a role in the pathogenesis of Alzheimer's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789838/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Jae-Eun -- Lim, Miranda M -- Bateman, Randall J -- Lee, James J -- Smyth, Liam P -- Cirrito, John R -- Fujiki, Nobuhiro -- Nishino, Seiji -- Holtzman, David M -- AG025824/AG/NIA NIH HHS/ -- AG029524/AG/NIA NIH HHS/ -- AG030946/AG/NIA NIH HHS/ -- K01 AG029524/AG/NIA NIH HHS/ -- K01 AG029524-03/AG/NIA NIH HHS/ -- K23 AG030946/AG/NIA NIH HHS/ -- K23 AG030946-03/AG/NIA NIH HHS/ -- MH072525/MH/NIMH NIH HHS/ -- NS065667/NS/NINDS NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-09/DK/NIDDK NIH HHS/ -- P30 NS057105/NS/NINDS NIH HHS/ -- P30 NS057105-04/NS/NINDS NIH HHS/ -- P50 AG005681/AG/NIA NIH HHS/ -- R01 AG025824/AG/NIA NIH HHS/ -- R01 AG025824-03/AG/NIA NIH HHS/ -- R01 MH072525/MH/NIMH NIH HHS/ -- R01 MH072525-04/MH/NIMH NIH HHS/ -- R01 NS065667/NS/NINDS NIH HHS/ -- R01 NS065667-02/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):1005-7. doi: 10.1126/science.1180962. Epub 2009 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Washington University, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19779148" target="_blank"〉PubMed〈/a〉
    Keywords: Acetamides/pharmacology ; Alzheimer Disease/metabolism/*physiopathology ; Amyloid beta-Peptides/cerebrospinal fluid/*metabolism ; Animals ; Antigens, Surface/metabolism ; Circadian Rhythm ; Disease Models, Animal ; Extracellular Fluid/*metabolism ; Female ; Hippocampus/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/administration & dosage/*metabolism ; Isoquinolines/pharmacology ; Light ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuropeptides/administration & dosage/*metabolism ; Orexin Receptors ; Orexins ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Neuropeptide/metabolism ; Signal Transduction ; *Sleep ; Sleep Deprivation ; *Wakefulness
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 27
    facet.materialart.
    Unknown
    Immunology. Dangers in and out (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bianchi, Marco E -- Manfredi, Angelo A -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1683-4. doi: 10.1126/science.1172794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉San Raffaele University, Faculty of Medicine, and San Raffaele Scientific Institute, via Olgettina 58, 20132 Milano, Italy. bianchi.marco@hsr.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325105" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD24/immunology/metabolism ; Autoimmunity ; HMGB1 Protein/metabolism ; Immunity ; *Immunity, Innate ; Infection/*immunology ; Inflammation/*immunology ; Lectins/immunology/metabolism ; Liver/*immunology/pathology ; Mice ; Necrosis/chemically induced/immunology ; Receptors, Antigen, B-Cell/immunology/metabolism ; Receptors, Pattern Recognition/immunology/metabolism ; Signal Transduction ; Wounds and Injuries/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 28
    facet.materialart.
    Unknown
    In vivo analysis of dendritic cell development and homeostasis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: Dendritic cells (DCs) in lymphoid tissue arise from precursors that also produce monocytes and plasmacytoid DCs (pDCs). Where DC and monocyte lineage commitment occurs and the nature of the DC precursor that migrates from the bone marrow to peripheral lymphoid organs are unknown. We show that DC development progresses from the macrophage and DC precursor to common DC precursors that give rise to pDCs and classical spleen DCs (cDCs), but not monocytes, and finally to committed precursors of cDCs (pre-cDCs). Pre-cDCs enter lymph nodes through and migrate along high endothelial venules and later disperse and integrate into the DC network. Further cDC development involves cell division, which is controlled in part by regulatory T cells and fms-like tyrosine kinase receptor-3.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803315/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Kang -- Victora, Gabriel D -- Schwickert, Tanja A -- Guermonprez, Pierre -- Meredith, Matthew M -- Yao, Kaihui -- Chu, Fei-Fan -- Randolph, Gwendalyn J -- Rudensky, Alexander Y -- Nussenzweig, Michel -- P01 AI051573/AI/NIAID NIH HHS/ -- P01 AI051573-010004/AI/NIAID NIH HHS/ -- P01 AI051573-020004/AI/NIAID NIH HHS/ -- P01 AI051573-030004/AI/NIAID NIH HHS/ -- P01 AI051573-040004/AI/NIAID NIH HHS/ -- P01 AI051573-050004/AI/NIAID NIH HHS/ -- P01 AI051573-060004/AI/NIAID NIH HHS/ -- P01 AI051573-069005/AI/NIAID NIH HHS/ -- P01 AI051573-070004/AI/NIAID NIH HHS/ -- P01 AI051573-079005/AI/NIAID NIH HHS/ -- P01 AI051573-080004/AI/NIAID NIH HHS/ -- P01 AI051573-089005/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):392-7. doi: 10.1126/science.1170540. Epub 2009 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, New York, NY 10065, USA. liuk@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286519" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Blood Vessels/cytology ; Bone Marrow Cells/cytology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Movement ; Cell Shape ; Dendritic Cells/*cytology/immunology/physiology ; Homeostasis ; Lymph Nodes/blood supply/cytology/immunology ; Lymphoid Tissue/blood supply/*cytology/immunology ; Macrophages/cytology ; Mice ; Monocytes/*cytology ; Myeloid Progenitor Cells/*cytology/physiology ; Parabiosis ; Signal Transduction ; Spleen/cytology/immunology ; T-Lymphocytes, Regulatory/physiology ; Venules/cytology ; fms-Like Tyrosine Kinase 3/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 29
    facet.materialart.
    Unknown
    Insulin resistance. Prosperity's plague (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, Gary -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):256-60. doi: 10.1126/science.325_256.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19608888" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/metabolism ; Adipose Tissue/metabolism ; Animals ; Chronic Disease ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Diglycerides/metabolism ; Fatty Acids/blood/metabolism ; Glucose/metabolism ; Humans ; Inflammation/*physiopathology ; Insulin/*physiology ; *Insulin Resistance ; *Lipid Metabolism ; Liver/metabolism ; Muscles/metabolism ; Obesity/physiopathology ; Receptor, Insulin/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 30
    facet.materialart.
    Unknown
    How telomeres solve the end-protection problem (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: The ends of eukaryotic chromosomes have the potential to be mistaken for damaged or broken DNA and must therefore be protected from cellular DNA damage response pathways. Otherwise, cells might permanently arrest in the cell cycle, and attempts to "repair" the chromosome ends would have devastating consequences for genome integrity. This end-protection problem is solved by protein-DNA complexes called telomeres. Studies of mammalian cells have recently uncovered the mechanism by which telomeres disguise the chromosome ends. Comparison to unicellular eukaryotes reveals key differences in the DNA damage response systems that inadvertently threaten chromosome ends. Telomeres appear to be tailored to these variations, explaining their variable structure and composition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819049/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819049/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- CA076027/CA/NCI NIH HHS/ -- DP1 OD000379/OD/NIH HHS/ -- DP1 OD000379-01/OD/NIH HHS/ -- DP1 OD000379-02/OD/NIH HHS/ -- DP1 OD000379-03/OD/NIH HHS/ -- DP1 OD000379-04/OD/NIH HHS/ -- DP1 OD000379-05/OD/NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 CA076027/CA/NCI NIH HHS/ -- R01 CA076027-02/CA/NCI NIH HHS/ -- R01 CA076027-03/CA/NCI NIH HHS/ -- R01 CA076027-04/CA/NCI NIH HHS/ -- R01 CA076027-05A1/CA/NCI NIH HHS/ -- R01 CA076027-06/CA/NCI NIH HHS/ -- R01 CA076027-07/CA/NCI NIH HHS/ -- R01 CA076027-08/CA/NCI NIH HHS/ -- R01 CA076027-09/CA/NCI NIH HHS/ -- R01 CA076027-10/CA/NCI NIH HHS/ -- R01 CA076027-11/CA/NCI NIH HHS/ -- R01 CA076027-11S1/CA/NCI NIH HHS/ -- R01 CA076027-12/CA/NCI NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):948-52. doi: 10.1126/science.1170633.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@mail.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes/physiology ; Chromosomes, Mammalian/*physiology/ultrastructure ; Ciliophora/genetics/metabolism ; DNA/biosynthesis/*metabolism ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/metabolism ; Humans ; Repetitive Sequences, Nucleic Acid ; Signal Transduction ; Telomerase/metabolism ; Telomere/*physiology/ultrastructure ; Telomere-Binding Proteins/*metabolism ; Telomeric Repeat Binding Protein 2/metabolism ; Yeasts/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 31
    facet.materialart.
    Unknown
    Induced chromosomal proximity and gene fusions in prostate cancer (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-26
    Description: Gene fusions play a critical role in cancer progression. The mechanisms underlying their genesis and cell type specificity are not well understood. About 50% of human prostate cancers display a gene fusion involving the 5' untranslated region of TMPRSS2, an androgen-regulated gene, and the protein-coding sequences of ERG, which encodes an erythroblast transformation-specific (ETS) transcription factor. By studying human prostate cancer cells with fluorescence in situ hybridization, we show that androgen signaling induces proximity of the TMPRSS2 and ERG genomic loci, both located on chromosome 21q22.2. Subsequent exposure of the cells to gamma irradiation, which causes DNA double-strand breaks, facilitates the formation of the TMPRSS2-ERG gene fusion. These results may help explain why TMPRSS2-ERG fusions are restricted to the prostate, which is dependent on androgen signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935583/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935583/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, Ram-Shankar -- Tomlins, Scott A -- Callahan, Kaitlin -- Ghosh, Aparna -- Nyati, Mukesh K -- Varambally, Sooryanarayana -- Palanisamy, Nallasivam -- Chinnaiyan, Arul M -- P50 CA069568/CA/NCI NIH HHS/ -- P50 CA069568-11S10020/CA/NCI NIH HHS/ -- P50CA69568/CA/NCI NIH HHS/ -- R01 CA132874/CA/NCI NIH HHS/ -- R01 CA132874-01A1/CA/NCI NIH HHS/ -- R01CA132874/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1230. doi: 10.1126/science.1178124. Epub 2009 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19933109" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Chromosome Aberrations ; Chromosomes, Human, Pair 21/*genetics/physiology ; DNA Breaks, Double-Stranded ; Dihydrotestosterone/*metabolism/pharmacology ; Humans ; In Situ Hybridization, Fluorescence ; Male ; *Oncogene Fusion ; Oncogene Proteins, Fusion/*genetics ; Prostatic Neoplasms/*genetics ; Receptors, Androgen/metabolism ; Serine Endopeptidases/*genetics ; Signal Transduction ; Trans-Activators/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 32
    facet.materialart.
    Unknown
    Input-specific spine entry of soma-derived Vesl-1S protein conforms to synaptic tagging (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: Late-phase synaptic plasticity depends on the synthesis of new proteins that must function only in the activated synapses. The synaptic tag hypothesis requires input-specific functioning of these proteins after undirected transport. Confirmation of this hypothesis requires specification of a biochemical tagging activity and an example protein that behaves as the hypothesis predicts. We found that in rat neurons, soma-derived Vesl-1S (Homer-1a) protein, a late-phase plasticity-related synaptic protein, prevailed in every dendrite and did not enter spines. N-methyl-d-aspartate receptor activation triggered input-specific spine entry of Vesl-1S proteins, which met many criteria for synaptic tagging. These results suggest that Vesl-1S supports the hypothesis and that the activity-dependent regulation of spine entry functions as a synaptic tag.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Daisuke -- Ozawa, Fumiko -- Inokuchi, Kaoru -- New York, N.Y. -- Science. 2009 May 15;324(5929):904-9. doi: 10.1126/science.1171498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mitsubishi Kagaku Institute of Life Sciences (MITILS), 11 Minamiooya, Machida, Tokyo 194-8511, Japan. dada@mitils.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; Dendrites/*metabolism ; Dendritic Spines/*metabolism/ultrastructure ; Hippocampus/cytology/metabolism ; Mice ; *Neuronal Plasticity ; Plasmids ; Protein Transport ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Synapses/*metabolism ; Synaptic Transmission ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 33
    facet.materialart.
    Unknown
    Hormone (dis)harmony moulds plant health and disease (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-09
    Description: Diseased plants often display phenotypes consistent with hormone perturbations. We review recent data that have revealed roles in plant-microbe interactions for cellular components and signaling molecules that previously were associated only with hormone signaling. A better understanding of cross-talk between hormonal and defense signaling pathways should reveal new potential targets for microbial effectors that attenuate host resistance mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grant, Murray R -- Jones, Jonathan D G -- BB/C514115/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 May 8;324(5928):750-2. doi: 10.1126/science.1173771.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biosciences, University of Exeter, Exeter EX4 4QD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423816" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/metabolism ; Bacteria/metabolism/*pathogenicity ; Cyclopentanes/metabolism ; Ethylenes/metabolism ; Fungi/metabolism/*pathogenicity ; Gene Expression Regulation, Plant ; Gibberellins/metabolism ; *Host-Pathogen Interactions ; Indoleacetic Acids/metabolism ; Oomycetes/pathogenicity ; Oxylipins/metabolism ; Plant Diseases/*microbiology ; Plant Growth Regulators/*metabolism ; Plant Proteins/metabolism ; Plants/genetics/*metabolism/*microbiology ; Repressor Proteins/metabolism ; Salicylic Acid/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 34
    facet.materialart.
    Unknown
    Reprogramming plant cells for endosymbiosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-09
    Description: The establishment of arbuscular mycorrhizal (AM) symbioses, formed by most flowering plants in association with glomeromycotan fungi, and the root-nodule (RN) symbiosis, formed by legume plants and rhizobial bacteria, requires an ongoing molecular dialogue that underpins the reprogramming of root cells for compatibility. In both endosymbioses, there are distinct phases to the interaction, including a presymbiotic anticipation phase and, subsequently, an intraradical accommodation of the microsymbiont. Maintenance of the endosymbiosis then depends on reciprocal nutrient exchange with the microsymbiont-obtaining plant photosynthates in exchange for mineral nutrients: enhanced phosphate and nitrogen uptake from AM fungi and fixed nitrogen from rhizobia. Despite the taxonomically distinct groups of symbionts, commonalities are observed in the signaling components and the modulation of host cell responses in both AM and RN symbioses, reflecting common mechanisms for plant cell reprogramming during endosymbiosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oldroyd, Giles E D -- Harrison, Maria J -- Paszkowski, Uta -- BB/E003850/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 May 8;324(5928):753-4. doi: 10.1126/science.1171644.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Disease and Stress Biology, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423817" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacterial Physiological Phenomena ; Gene Expression Regulation, Plant ; Lipopolysaccharides/metabolism ; Mycorrhizae/growth & development/*physiology ; Nitrogen Fixation ; Plant Proteins/metabolism ; Plant Root Nodulation ; Plant Roots/metabolism ; Plants/genetics/*metabolism/*microbiology ; Rhizobiaceae/*physiology ; Root Nodules, Plant/*microbiology ; Signal Transduction ; *Symbiosis ; Transcription Factors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 35
    facet.materialart.
    Unknown
    GE Prize essay. The molecular basis of size differences (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crickmore, Michael A -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1360-1. doi: 10.1126/science.1184444.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics and Behavior, Rockefeller University, New York, NY 10065, USA. mcrickmore@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965749" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Awards and Prizes ; Drosophila Proteins/*genetics/*metabolism/*physiology ; Drosophila melanogaster/*anatomy & histology/genetics/metabolism ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Genes, Insect ; Homeodomain Proteins/*genetics/*physiology ; Organ Size ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Receptors, Cell Surface/genetics/metabolism ; Signal Transduction ; Transcription Factors/*genetics/*physiology ; Wings, Animal/*anatomy & histology/cytology/growth & development/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 36
    facet.materialart.
    Unknown
    Neuroscience. Crossing the line (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kidd, Thomas -- New York, N.Y. -- Science. 2009 May 15;324(5929):893-4. doi: 10.1126/science.1174216.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Nevada, Reno, NV 89557, USA. tkidd@unr.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443775" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cell Adhesion Molecules/metabolism ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/*genetics/growth & development/metabolism ; *Gene Expression Regulation, Developmental ; Membrane Proteins/*genetics/metabolism ; Mutation ; Nerve Growth Factors/metabolism ; Nerve Tissue Proteins/*genetics/metabolism ; Nervous System/growth & development ; Neurons/*physiology ; Receptors, Cell Surface/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 37
    facet.materialart.
    Unknown
    Regulators of PP2C phosphatase activity function as abscisic acid sensors (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: The plant hormone abscisic acid (ABA) acts as a developmental signal and as an integrator of environmental cues such as drought and cold. Key players in ABA signal transduction include the type 2C protein phosphatases (PP2Cs) ABI1 and ABI2, which act by negatively regulating ABA responses. In this study, we identify interactors of ABI1 and ABI2 which we have named regulatory components of ABA receptor (RCARs). In Arabidopsis, RCARs belong to a family with 14 members that share structural similarity with class 10 pathogen-related proteins. RCAR1 was shown to bind ABA, to mediate ABA-dependent inactivation of ABI1 or ABI2 in vitro, and to antagonize PP2C action in planta. Other RCARs also mediated ABA-dependent regulation of ABI1 and ABI2, consistent with a combinatorial assembly of receptor complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Yue -- Szostkiewicz, Izabela -- Korte, Arthur -- Moes, Daniele -- Yang, Yi -- Christmann, Alexander -- Grill, Erwin -- New York, N.Y. -- Science. 2009 May 22;324(5930):1064-8. doi: 10.1126/science.1172408. Epub 2009 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lehrstuhl fur Botanik, Technische Universitat Munchen, Am Hochanger 4, D-85354 Freising, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407143" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*metabolism/pharmacology ; Amino Acid Sequence ; Arabidopsis/genetics/*metabolism/physiology ; Arabidopsis Proteins/antagonists & inhibitors/chemistry/genetics/*metabolism ; Binding Sites ; Carrier Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation, Plant ; Germination ; Molecular Sequence Data ; Phosphoprotein Phosphatases/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; Plant Roots/growth & development ; Plant Stomata/physiology ; Plants, Genetically Modified ; Point Mutation ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Stereoisomerism ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 38
    facet.materialart.
    Unknown
    Ventral tegmental area BDNF induces an opiate-dependent-like reward state in naive rats (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: The neural mechanisms underlying the transition from a drug-nondependent to a drug-dependent state remain elusive. Chronic exposure to drugs has been shown to increase brain-derived neurotrophic factor (BDNF) levels in ventral tegmental area (VTA) neurons. BDNF infusions into the VTA potentiate several behavioral effects of drugs, including psychomotor sensitization and cue-induced drug seeking. We found that a single infusion of BDNF into the VTA promotes a shift from a dopamine-independent to a dopamine-dependent opiate reward system, identical to that seen when an opiate-naive rat becomes dependent and withdrawn. This shift involves a switch in the gamma-aminobutyric acid type A (GABAA) receptors of VTA GABAergic neurons, from inhibitory to excitatory signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913611/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913611/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vargas-Perez, Hector -- Ting-A Kee, Ryan -- Walton, Christine H -- Hansen, D Micah -- Razavi, Rozita -- Clarke, Laura -- Bufalino, Mary Rose -- Allison, David W -- Steffensen, Scott C -- van der Kooy, Derek -- AA13666/AA/NIAAA NIH HHS/ -- R01 AA013666/AA/NIAAA NIH HHS/ -- R01 AA013666-09/AA/NIAAA NIH HHS/ -- R01 AA020919/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1732-4. doi: 10.1126/science.1168501. Epub 2009 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada. vargashector@yahoo.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Brain-Derived Neurotrophic Factor/administration & ; dosage/genetics/*metabolism/*pharmacology ; Conditioning (Psychology) ; Dopamine/physiology ; Dopamine Antagonists/administration & dosage/pharmacology ; Flupenthixol/administration & dosage/pharmacology ; GABA Agonists/pharmacology ; GABA Antagonists/pharmacology ; Heroin Dependence/metabolism ; Male ; Morphine/administration & dosage ; Muscimol/pharmacology ; Opioid-Related Disorders/*metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; *Reward ; Signal Transduction ; Substance Withdrawal Syndrome/metabolism ; Ventral Tegmental Area/drug effects/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 39
    facet.materialart.
    Unknown
    Trifurcate feed-forward regulation of age-dependent cell death involving miR164 in Arabidopsis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-21
    Description: Aging induces gradual yet massive cell death in higher organisms, including annual plants. Even so, the underlying regulatory mechanisms are barely known, despite the long-standing interest in this topic. Here, we demonstrate that ORE1, which is a NAC (NAM, ATAF, and CUC) transcription factor, positively regulates aging-induced cell death in Arabidopsis leaves. ORE1 expression is up-regulated concurrently with leaf aging by EIN2 but is negatively regulated by miR164. miR164 expression gradually decreases with aging through negative regulation by EIN2, which leads to the elaborate up-regulation of ORE1 expression. However, EIN2 still contributes to aging-induced cell death in the absence of ORE1. The trifurcate feed-forward pathway involving ORE1, miR164, and EIN2 provides a highly robust regulation to ensure that aging induces cell death in Arabidopsis leaves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jin Hee -- Woo, Hye Ryun -- Kim, Jeongsik -- Lim, Pyung Ok -- Lee, In Chul -- Choi, Seung Hee -- Hwang, Daehee -- Nam, Hong Gil -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1053-7. doi: 10.1126/science.1166386.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Life Sciences, Pohang University of Science and Technology, Hyoja-dong, Pohang, Kyungbuk, 790-784, Republic of Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19229035" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; *Apoptosis ; Arabidopsis/cytology/genetics/*physiology ; Arabidopsis Proteins/genetics/*physiology ; Down-Regulation ; Gene Expression Regulation, Plant ; Genes, Plant ; MicroRNAs/genetics/*physiology ; Mutation ; Plant Leaves/cytology/*physiology ; Plants, Genetically Modified ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/*physiology ; Receptors, Cell Surface/genetics/*physiology ; Signal Transduction ; Transcription Factors/genetics/*physiology ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 40
    facet.materialart.
    Unknown
    A role for the CHC22 clathrin heavy-chain isoform in human glucose metabolism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Intracellular trafficking of the glucose transporter GLUT4 from storage compartments to the plasma membrane is triggered in muscle and fat during the body's response to insulin. Clathrin is involved in intracellular trafficking, and in humans, the clathrin heavy-chain isoform CHC22 is highly expressed in skeletal muscle. We found a role for CHC22 in the formation of insulin-responsive GLUT4 compartments in human muscle and adipocytes. CHC22 also associated with expanded GLUT4 compartments in muscle from type 2 diabetic patients. Tissue-specific introduction of CHC22 in mice, which have only a pseudogene for this protein, caused aberrant localization of GLUT4 transport pathway components in their muscle, as well as features of diabetes. Thus, CHC22-dependent membrane trafficking constitutes a species-restricted pathway in human muscle and fat with potential implications for type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassilopoulos, Stephane -- Esk, Christopher -- Hoshino, Sachiko -- Funke, Birgit H -- Chen, Chih-Ying -- Plocik, Alex M -- Wright, Woodring E -- Kucherlapati, Raju -- Brodsky, Frances M -- GM038093/GM/NIGMS NIH HHS/ -- HD47863/HD/NICHD NIH HHS/ -- R01 GM038093/GM/NIGMS NIH HHS/ -- R01 GM038093-19/GM/NIGMS NIH HHS/ -- R01 GM038093-19S1/GM/NIGMS NIH HHS/ -- R01 GM038093-20A1/GM/NIGMS NIH HHS/ -- R01 HD047863/HD/NICHD NIH HHS/ -- R01 HD047863-01/HD/NICHD NIH HHS/ -- R01 HD047863-02/HD/NICHD NIH HHS/ -- R01 HD047863-03/HD/NICHD NIH HHS/ -- R01 HD047863-04/HD/NICHD NIH HHS/ -- R01 HD047863-05/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 May 29;324(5931):1192-6. doi: 10.1126/science.1171529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering and Therapeutic Sciences, University of California, School of Pharmacy, San Francisco (UCSF), San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478182" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/*metabolism/ultrastructure ; Animals ; Blood Glucose/metabolism ; Cell Differentiation ; Cell Line ; Cell Membrane/metabolism ; Clathrin/chemistry/*metabolism ; Clathrin Heavy Chains ; Clathrin-Coated Vesicles/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Glucose/*metabolism ; Glucose Transporter Type 4/*metabolism ; Humans ; Insulin/blood/pharmacology ; Mice ; Mice, Transgenic ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/*metabolism/ultrastructure ; Myoblasts/cytology/metabolism/ultrastructure ; Protein Isoforms/chemistry/metabolism ; Protein Transport ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 41
    facet.materialart.
    Unknown
    Two chemoreceptors mediate developmental effects of dauer pheromone in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Intraspecific chemical communication is mediated by signals called pheromones. Caenorhabditis elegans secretes a mixture of small molecules (collectively termed dauer pheromone) that regulates entry into the alternate dauer larval stage and also modulates adult behavior via as yet unknown receptors. Here, we identify two heterotrimeric GTP-binding protein (G protein)-coupled receptors (GPCRs) that mediate dauer formation in response to a subset of dauer pheromone components. The SRBC-64 and SRBC-66 GPCRs are members of the large Caenorhabditis-specific SRBC subfamily and are expressed in the ASK chemosensory neurons, which are required for pheromone-induced dauer formation. Expression of both, but not each receptor alone, confers pheromone-mediated effects on heterologous cells. Identification of dauer pheromone receptors will allow a better understanding of the signaling cascades that transduce the context-dependent effects of ecologically important chemical signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448937/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kyuhyung -- Sato, Koji -- Shibuya, Mayumi -- Zeiger, Danna M -- Butcher, Rebecca A -- Ragains, Justin R -- Clardy, Jon -- Touhara, Kazushige -- Sengupta, Piali -- F32 GM077943/GM/NIGMS NIH HHS/ -- P30 NS045713/NS/NINDS NIH HHS/ -- P30 NS45713/NS/NINDS NIH HHS/ -- R01 CA024487/CA/NCI NIH HHS/ -- R01 CA24487/CA/NCI NIH HHS/ -- R01 GM056223/GM/NIGMS NIH HHS/ -- R01 GM56223/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):994-8. doi: 10.1126/science.1176331. Epub 2009 Oct 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/*growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Calcium/metabolism ; Cell Line ; Chemoreceptor Cells/metabolism ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; GTP-Binding Protein alpha Subunits, Gi-Go/physiology ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; Hexoses/chemistry/physiology ; Humans ; Mutation ; Pheromones/*physiology ; Receptors, G-Protein-Coupled ; Reproduction ; Signal Transduction ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 42
    facet.materialart.
    Unknown
    Medicine. A reinnervating microRNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Robert H -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1494-5. doi: 10.1126/science.1183842.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology, Biochemistry and Molecular Pharmacology and Program in Neuroscience, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. robert.brown@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007892" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Binding Sites ; Carrier Proteins/metabolism ; Disease Models, Animal ; Histone Deacetylases/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Muscle Cells/enzymology ; Muscle Denervation ; Muscle, Skeletal/innervation/metabolism ; Myostatin/genetics ; Neuromuscular Junction/*pathology/*physiology ; RNA Interference ; Sequence Analysis, RNA ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 43
    facet.materialart.
    Unknown
    gamma-Secretase heterogeneity in the Aph1 subunit: relevance for Alzheimer's disease (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: The gamma-secretase complex plays a role in Alzheimer's disease and cancer progression. The development of clinically useful inhibitors, however, is complicated by the role of the gamma-secretase complex in regulated intramembrane proteolysis of Notch and other essential proteins. Different gamma-secretase complexes containing different Presenilin or Aph1 protein subunits are present in various tissues. Here we show that these complexes have heterogeneous biochemical and physiological properties. Specific inactivation of the Aph1B gamma-secretase in a mouse Alzheimer's disease model led to improvements of Alzheimer's disease-relevant phenotypic features without any Notch-related side effects. The Aph1B complex contributes to total gamma-secretase activity in the human brain, and thus specific targeting of Aph1B-containing gamma-secretase complexes may help generate less toxic therapies for Alzheimer's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2740474/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2740474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Serneels, Lutgarde -- Van Biervliet, Jerome -- Craessaerts, Katleen -- Dejaegere, Tim -- Horre, Katrien -- Van Houtvin, Tine -- Esselmann, Hermann -- Paul, Sabine -- Schafer, Martin K -- Berezovska, Oksana -- Hyman, Bradley T -- Sprangers, Ben -- Sciot, Raf -- Moons, Lieve -- Jucker, Mathias -- Yang, Zhixiang -- May, Patrick C -- Karran, Eric -- Wiltfang, Jens -- D'Hooge, Rudi -- De Strooper, Bart -- AG 13579/AG/NIA NIH HHS/ -- AG026593/AG/NIA NIH HHS/ -- P01 AG015379/AG/NIA NIH HHS/ -- P01 AG015379-110009/AG/NIA NIH HHS/ -- P01AG015379/AG/NIA NIH HHS/ -- R01 AG026593/AG/NIA NIH HHS/ -- R01 AG026593-01A1/AG/NIA NIH HHS/ -- R01AG026593/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):639-42. doi: 10.1126/science.1171176. Epub 2009 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department for Molecular and Developmental Genetics, VIB, KULeuven, Herestraat 49, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299585" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/*metabolism ; Amyloid Precursor Protein Secretases/antagonists & ; inhibitors/*chemistry/genetics/*metabolism ; Amyloid beta-Peptides/analysis/chemistry/*metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Brain/*metabolism ; Disease Models, Animal ; Endopeptidases/chemistry/genetics/*metabolism ; Female ; Humans ; Maze Learning ; Membrane Proteins/metabolism ; Memory ; Mice ; Neurons/metabolism ; Peptide Fragments/analysis/metabolism ; Peptide Hydrolases/metabolism ; Presenilin-1/chemistry/genetics/metabolism ; Protein Subunits/chemistry/metabolism ; Receptor, Notch1/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 44
    facet.materialart.
    Unknown
    Induction of synaptic long-term potentiation after opioid withdrawal (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: mu-Opioid receptor (MOR) agonists represent the gold standard for the treatment of severe pain but may paradoxically also enhance pain sensitivity, that is, lead to opioid-induced hyperalgesia (OIH). We show that abrupt withdrawal from MOR agonists induces long-term potentiation (LTP) at the first synapse in pain pathways. Induction of opioid withdrawal LTP requires postsynaptic activation of heterotrimeric guanine nucleotide-binding proteins and N-methyl-d-aspartate receptors and a rise of postsynaptic calcium concentrations. In contrast, the acute depression by opioids is induced presynaptically at these synapses. Withdrawal LTP can be prevented by tapered withdrawal and shares pharmacology and signal transduction pathways with OIH. These findings provide a previously unrecognized target to selectively combat pro-nociceptive effects of opioids without compromising opioid analgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drdla, Ruth -- Gassner, Matthias -- Gingl, Ewald -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2009 Jul 10;325(5937):207-10. doi: 10.1126/science.1171759.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19590003" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/administration & dosage/*adverse effects/pharmacology ; Animals ; Calcium/metabolism ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/administration & dosage/adverse ; effects/pharmacology ; Evoked Potentials ; GTP-Binding Proteins/metabolism ; Hyperalgesia/chemically induced ; *Long-Term Potentiation/drug effects ; Male ; Nerve Fibers, Unmyelinated/physiology ; Patch-Clamp Techniques ; Piperidines/administration & dosage/adverse effects/pharmacology ; Posterior Horn Cells/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Opioid, mu/*agonists ; Signal Transduction ; Substance Withdrawal Syndrome/*physiopathology ; Synapses/drug effects/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 45
    facet.materialart.
    Unknown
    Abscisic acid inhibits type 2C protein phosphatases via the PYR/PYL family of START proteins (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Type 2C protein phosphatases (PP2Cs) are vitally involved in abscisic acid (ABA) signaling. Here, we show that a synthetic growth inhibitor called pyrabactin functions as a selective ABA agonist. Pyrabactin acts through PYRABACTIN RESISTANCE 1 (PYR1), the founding member of a family of START proteins called PYR/PYLs, which are necessary for both pyrabactin and ABA signaling in vivo. We show that ABA binds to PYR1, which in turn binds to and inhibits PP2Cs. We conclude that PYR/PYLs are ABA receptors functioning at the apex of a negative regulatory pathway that controls ABA signaling by inhibiting PP2Cs. Our results illustrate the power of the chemical genetic approach for sidestepping genetic redundancy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827199/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827199/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Sang-Youl -- Fung, Pauline -- Nishimura, Noriyuki -- Jensen, Davin R -- Fujii, Hiroaki -- Zhao, Yang -- Lumba, Shelley -- Santiago, Julia -- Rodrigues, Americo -- Chow, Tsz-Fung F -- Alfred, Simon E -- Bonetta, Dario -- Finkelstein, Ruth -- Provart, Nicholas J -- Desveaux, Darrell -- Rodriguez, Pedro L -- McCourt, Peter -- Zhu, Jian-Kang -- Schroeder, Julian I -- Volkman, Brian F -- Cutler, Sean R -- 01GM59138/GM/NIGMS NIH HHS/ -- R01 GM060396/GM/NIGMS NIH HHS/ -- R01 GM060396-08/GM/NIGMS NIH HHS/ -- R01GM060396/GM/NIGMS NIH HHS/ -- U54GM074901/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1068-71. doi: 10.1126/science.1173041. Epub 2009 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany and Plant Sciences, University of California at Riverside, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407142" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/agonists/*metabolism ; Arabidopsis/enzymology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/*antagonists & inhibitors/genetics/*metabolism ; Genes, Plant ; Germination/drug effects ; Ligands ; Membrane Transport Proteins/genetics/*metabolism ; Mutation ; Naphthalenes/chemistry/metabolism/*pharmacology ; Phosphoprotein Phosphatases/*antagonists & inhibitors/metabolism ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Seeds/growth & development/metabolism ; Signal Transduction ; Sulfonamides/chemistry/metabolism/*pharmacology ; Two-Hybrid System Techniques
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 46
    facet.materialart.
    Unknown
    Biomedicine. A new view on--and hope for--an old disease (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cahoon, Lauren -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):203-5. doi: 10.1126/science.323.5911.203.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131605" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/pathology/physiopathology ; Cognition Disorders/drug therapy/genetics/pathology/physiopathology ; Epilepsy/etiology ; Humans ; *Mental Disorders/drug therapy/genetics/pathology/physiopathology ; Neurons/physiology ; Protein Kinases/metabolism ; Signal Transduction ; Sirolimus/*therapeutic use ; TOR Serine-Threonine Kinases ; *Tuberous Sclerosis/drug therapy/genetics/pathology/physiopathology ; Tumor Suppressor Proteins/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 47
    facet.materialart.
    Unknown
    Arterial-venous segregation by selective cell sprouting: an alternative mode of blood vessel formation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: Blood vessels form de novo (vasculogenesis) or upon sprouting of capillaries from preexisting vessels (angiogenesis). With high-resolution imaging of zebrafish vascular development, we uncovered a third mode of blood vessel formation whereby the first embryonic artery and vein, two unconnected blood vessels, arise from a common precursor vessel. The first embryonic vein formed by selective sprouting of progenitor cells from the precursor vessel, followed by vessel segregation. These processes were regulated by the ligand EphrinB2 and its receptor EphB4, which are expressed in arterial-fated and venous-fated progenitors, respectively, and interact to orient the direction of progenitor migration. Thus, directional control of progenitor migration drives arterial-venous segregation and generation of separate parallel vessels from a single precursor vessel, a process essential for vascular development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865998/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herbert, Shane P -- Huisken, Jan -- Kim, Tyson N -- Feldman, Morri E -- Houseman, Benjamin T -- Wang, Rong A -- Shokat, Kevan M -- Stainier, Didier Y R -- 082719/Wellcome Trust/United Kingdom -- HL54737/HL/NHLBI NIH HHS/ -- R01 HL054737/HL/NHLBI NIH HHS/ -- R01 HL054737-14/HL/NHLBI NIH HHS/ -- R01 HL075033/HL/NHLBI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):294-8. doi: 10.1126/science.1178577.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Programs in Developmental Biology, Genetics and Human Genetics, Cardiovascular Research Institute, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Aorta/cytology/embryology ; Arteries/cytology/*embryology ; Cell Movement ; Endothelial Cells/cytology/*physiology ; Ephrin-B2/*metabolism ; *Morphogenesis ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, EphB4/*metabolism ; Receptors, Notch/metabolism ; Signal Transduction ; Stem Cells/cytology/*physiology ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; Vascular Endothelial Growth Factor Receptor-3/metabolism ; Veins/cytology/*embryology ; Zebrafish ; Zebrafish Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 48
    facet.materialart.
    Unknown
    Starvation protects germline stem cells and extends reproductive longevity in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-29
    Description: The study of starvation-resistant biological programs has elucidated numerous mechanisms influencing aging. Here we present the discovery and characterization of starvation-induced adult reproductive diapause (ARD) in Caenorhabditis elegans. ARD differs from the C. elegans dauer diapause in that it enables sexually mature adults to delay reproductive onset 15-fold and extend total adult life span at least threefold. The effectiveness of ARD requires apoptotic death of the entire germ line, except for a small population of protected germline stem cells (GSCs). When feeding is resumed, surviving GSCs regenerate a new germ line capable of offspring production near the level of nonstarved animals. The starvation-sensing nuclear receptor NHR-49 is required for ARD entry and recovery. Our findings establish mechanisms for preserving stem cell potency and reproductive potential during prolonged starvation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angelo, Giana -- Van Gilst, Marc R -- GM080895-02/GM/NIGMS NIH HHS/ -- R01 DK079273/DK/NIDDK NIH HHS/ -- RDK079273A/PHS HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):954-8. doi: 10.1126/science.1178343.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713489" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Apoptosis ; Caenorhabditis elegans/embryology/genetics/*growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/*physiology ; Caspases/genetics/physiology ; Embryonic Development ; Germ Cells/cytology/*physiology ; Larva/growth & development/physiology ; Longevity ; Mutation ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; Reproduction ; Signal Transduction ; Starvation ; Stem Cells/*physiology ; Stress, Physiological
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 49
    facet.materialart.
    Unknown
    PAN1: a receptor-like protein that promotes polarization of an asymmetric cell division in maize (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: Polarization of cell division is essential for eukaryotic development, but little is known about how this is accomplished in plants. The formation of stomatal complexes in maize involves the polarization of asymmetric subsidiary mother cell (SMC) divisions toward the adjacent guard mother cell (GMC), apparently under the influence of a GMC-derived signal. We found that the maize pan1 gene promotes the premitotic polarization of SMCs and encodes a leucine-rich repeat receptor-like protein that becomes localized in SMCs at sites of GMC contact. PAN1 has an inactive kinase domain but is required for the accumulation of a membrane-associated phosphoprotein, suggesting a function for PAN1 in signal transduction. Our findings implicate PAN1 in the transmission of an extrinsic signal that polarizes asymmetric SMC divisions toward GMCs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cartwright, Heather N -- Humphries, John A -- Smith, Laurie G -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):649-51. doi: 10.1126/science.1161686.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Cell and Developmental Biology, University of California San Diego, 9500 Gilman Drive, San Diego, CA 92093-0116, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179535" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Amino Acid Sequence ; Cell Division ; Cell Nucleus/ultrastructure ; Cell Polarity ; Cues ; Genes, Plant ; Molecular Sequence Data ; Phosphorylation ; Plant Leaves/*cytology ; Plant Proteins/chemistry/genetics/*metabolism ; Plant Stomata/*cytology/genetics/growth & development/metabolism ; Protein Structure, Tertiary ; Signal Transduction ; Zea mays/*cytology/genetics/growth & development/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 50
    facet.materialart.
    Unknown
    Proteasomal regulation of the hypoxic response modulates aging in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-18
    Description: The Caenorhabditis elegans von Hippel-Lindau tumor suppressor homolog VHL-1 is a cullin E3 ubiquitin ligase that negatively regulates the hypoxic response by promoting ubiquitination and degradation of the hypoxic response transcription factor HIF-1. Here, we report that loss of VHL-1 significantly increased life span and enhanced resistance to polyglutamine and beta-amyloid toxicity. Deletion of HIF-1 was epistatic to VHL-1, indicating that HIF-1 acts downstream of VHL-1 to modulate aging and proteotoxicity. VHL-1 and HIF-1 control longevity by a mechanism distinct from both dietary restriction and insulin-like signaling. These findings define VHL-1 and the hypoxic response as an alternative longevity and protein homeostasis pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737476/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737476/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mehta, Ranjana -- Steinkraus, Katherine A -- Sutphin, George L -- Ramos, Fresnida J -- Shamieh, Lara S -- Huh, Alexander -- Davis, Christina -- Chandler-Brown, Devon -- Kaeberlein, Matt -- 1R01AG031108-01/AG/NIA NIH HHS/ -- P30AG013280/AG/NIA NIH HHS/ -- R01 AG031108/AG/NIA NIH HHS/ -- R01 AG031108-01A1/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2009 May 29;324(5931):1196-8. doi: 10.1126/science.1173507. Epub 2009 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372390" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Amyloid beta-Peptides/toxicity ; Animals ; Caenorhabditis elegans/genetics/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Caloric Restriction ; Cullin Proteins/genetics/*metabolism ; Female ; Fertility ; Gene Expression Regulation ; Homeostasis ; Insulin/metabolism ; Longevity/physiology ; Male ; Models, Animal ; Oxygen/*physiology ; Peptides/toxicity ; Proteasome Endopeptidase Complex/*metabolism ; RNA Interference ; Receptor, Insulin/genetics/metabolism ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 51
    facet.materialart.
    Unknown
    IL-21 is required to control chronic viral infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-09
    Description: CD4+ and CD8+ T cell functions are rapidly aborted during chronic infection, preventing viral clearance. CD4+ T cell help is required throughout chronic infection so as to sustain CD8+ T cell responses; however, the necessary factor(s) provided by CD4+ T cells are currently unknown. Using a mouse model of chronic viral infection, we demonstrated that interleukin-21 (IL-21) is an essential component of CD4+ T cell help. In the absence of IL-21 signaling, despite elevated CD4+ T cell responses, CD8+ T cell responses are severely impaired. CD8+ T cells directly require IL-21 to avoid deletion, maintain immunity, and resolve persistent infection. Thus, IL-21 specifically sustains CD8+ T cell effector activity and provides a mechanism of CD4+ T cell help during chronic viral infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830017/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830017/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elsaesser, Heidi -- Sauer, Karsten -- Brooks, David G -- AI070845/AI/NIAID NIH HHS/ -- AI077012/AI/NIAID NIH HHS/ -- AI082975/AI/NIAID NIH HHS/ -- R01 AI085043/AI/NIAID NIH HHS/ -- R21 AI077012/AI/NIAID NIH HHS/ -- R21 AI077012-03/AI/NIAID NIH HHS/ -- U01 AI082975/AI/NIAID NIH HHS/ -- U01 AI082975-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 19;324(5934):1569-72. doi: 10.1126/science.1174182. Epub 2009 May 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology, and Molecular Genetics and University of California, Los Angeles (UCLA) AIDS Institute, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Chronic Disease ; Interleukins/genetics/*immunology ; Lymphocyte Activation ; Lymphocyte Depletion ; Lymphocytic Choriomeningitis/*immunology ; Lymphocytic choriomeningitis virus ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Signal Transduction ; Virus Diseases/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 52
    facet.materialart.
    Unknown
    RNA Pol II accumulates at promoters of growth genes during developmental arrest (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: When Caenorhabditis elegans larvae hatch from the egg case in the absence of food, their development is arrested (L1 arrest), and they show increased stress resistance until food becomes available. To study nutritional control of larval development, we analyzed growth and gene expression profiles during L1 arrest and recovery. Larvae that were fed responded relatively slowly to starvation compared with the rapid response of arrested larvae to feeding. Chromatin immunoprecipitation of RNA polymerase II (Pol II) followed by deep sequencing showed that during L1 arrest, Pol II continued transcribing starvation-response genes, but the enzyme accumulated on the promoters of growth and development genes. In response to feeding, promoter accumulation decreased, and elongation and messenger RNA levels increased. Therefore, accumulation of Pol II at promoters anticipates nutritionally controlled gene expression during C. elegans development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baugh, L Ryan -- Demodena, John -- Sternberg, Paul W -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):92-4. doi: 10.1126/science.1169628. Epub 2009 Feb 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/*growth & development/metabolism ; Chromatin Immunoprecipitation ; Cluster Analysis ; Escherichia coli ; Food ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Helminth ; Nutritional Physiological Phenomena ; Oligonucleotide Array Sequence Analysis ; Principal Component Analysis ; *Promoter Regions, Genetic ; RNA Polymerase II/*metabolism ; RNA, Helminth/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; Starvation ; Transcription, Genetic ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 53
    facet.materialart.
    Unknown
    Evolutionary development of the middle ear in Mesozoic therian mammals (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: The definitive mammalian middle ear (DMME) is defined by the loss of embryonic Meckel's cartilage and disconnection of the middle ear from the mandible in adults. It is a major feature distinguishing living mammals from nonmammalian vertebrates. We report a Cretaceous trechnotherian mammal with an ossified Meckel's cartilage in the adult, showing that homoplastic evolution of the DMME occurred in derived therian mammals, besides the known cases of eutriconodonts. The mandible with ossified Meckel's cartilage appears to be paedomorphic. Reabsorption of embryonic Meckel's cartilage to disconnect the ear ossicles from the mandible is patterned by a network of genes and signaling pathways. This fossil suggests that developmental heterochrony and gene patterning are major mechanisms in homplastic evolution of the DMME.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ji, Qiang -- Luo, Zhe-Xi -- Zhang, Xingliao -- Yuan, Chong-Xi -- Xu, Li -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):278-81. doi: 10.1126/science.1178501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Geology, Chinese Academy of Geological Sciences, Beijing 100037, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cartilage/embryology/physiology ; Chondrogenesis ; Dentition ; Ear Ossicles/anatomy & histology/embryology ; *Ear, Middle/anatomy & histology/embryology ; Embryo, Mammalian/anatomy & histology ; *Fossils ; Gene Expression Regulation, Developmental ; Intercellular Signaling Peptides and Proteins/metabolism ; *Mammals/anatomy & histology/classification/embryology/genetics ; Mandible/anatomy & histology ; Mice ; Mice, Mutant Strains ; *Osteogenesis ; Phylogeny ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 54
    facet.materialart.
    Unknown
    Immunology. Dispensable but not irrelevant (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917045/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917045/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jia, Ting -- Pamer, Eric G -- P01 CA023766/CA/NCI NIH HHS/ -- P01 CA023766-320044/CA/NCI NIH HHS/ -- R01 AI080619/AI/NIAID NIH HHS/ -- R37 AI039031/AI/NIAID NIH HHS/ -- R37 AI039031-16/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):549-50. doi: 10.1126/science.1178329.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Sloan-Kettering Institute, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644100" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/blood ; Animals ; Antigens, Ly/metabolism ; Mice ; Monocytes/immunology/*physiology ; Myocardial Infarction/immunology/*pathology/*physiopathology ; Myocardium/*immunology/*pathology ; Receptors, CCR2/metabolism ; Receptors, Chemokine/metabolism ; Signal Transduction ; Spleen/cytology/*immunology ; Ventricular Remodeling
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 55
    facet.materialart.
    Unknown
    Activation of the PI3K pathway in cancer through inhibition of PTEN by exchange factor P-REX2a (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: PTEN (phosphatase and tensin homolog on chromosome 10) is a tumor suppressor whose cellular regulation remains incompletely understood. We identified phosphatidylinositol 3,4,5-trisphosphate RAC exchanger 2a (P-REX2a) as a PTEN-interacting protein. P-REX2a mRNA was more abundant in human cancer cells and significantly increased in tumors with wild-type PTEN that expressed an activated mutant of PIK3CA encoding the p110 subunit of phosphoinositide 3-kinase subunit alpha (PI3Kalpha). P-REX2a inhibited PTEN lipid phosphatase activity and stimulated the PI3K pathway only in the presence of PTEN. P-REX2a stimulated cell growth and cooperated with a PIK3CA mutant to promote growth factor-independent proliferation and transformation. Depletion of P-REX2a reduced amounts of phosphorylated AKT and growth in human cell lines with intact PTEN. Thus, P-REX2a is a component of the PI3K pathway that can antagonize PTEN in cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936784/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fine, Barry -- Hodakoski, Cindy -- Koujak, Susan -- Su, Tao -- Saal, Lao H -- Maurer, Matthew -- Hopkins, Benjamin -- Keniry, Megan -- Sulis, Maria Luisa -- Mense, Sarah -- Hibshoosh, Hanina -- Parsons, Ramon -- CA097403/CA/NCI NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- P01 CA097403-01A10003/CA/NCI NIH HHS/ -- P01 CA097403-06A1/CA/NCI NIH HHS/ -- R01 CA082783/CA/NCI NIH HHS/ -- R01 CA082783-06/CA/NCI NIH HHS/ -- R01 CA082783-07/CA/NCI NIH HHS/ -- R01 CA082783-08/CA/NCI NIH HHS/ -- R01 CA082783-09/CA/NCI NIH HHS/ -- R01 CA082783-10/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1261-5. doi: 10.1126/science.1173569.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics and Herbert Irving Comprehensive Cancer Center, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729658" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics/metabolism/pathology ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Female ; GTPase-Activating Proteins/genetics/*metabolism ; Guanine Nucleotide Exchange Factors ; Humans ; Male ; Mutation ; Neoplasms/genetics/*metabolism/pathology ; PTEN Phosphohydrolase/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 56
    facet.materialart.
    Unknown
    MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons, denervation of target muscles, muscle atrophy, and paralysis. Understanding ALS pathogenesis may require a fuller understanding of the bidirectional signaling between motor neurons and skeletal muscle fibers at neuromuscular synapses. Here, we show that a key regulator of this signaling is miR-206, a skeletal muscle-specific microRNA that is dramatically induced in a mouse model of ALS. Mice that are genetically deficient in miR-206 form normal neuromuscular synapses during development, but deficiency of miR-206 in the ALS mouse model accelerates disease progression. miR-206 is required for efficient regeneration of neuromuscular synapses after acute nerve injury, which probably accounts for its salutary effects in ALS. miR-206 mediates these effects at least in part through histone deacetylase 4 and fibroblast growth factor signaling pathways. Thus, miR-206 slows ALS progression by sensing motor neuron injury and promoting the compensatory regeneration of neuromuscular synapses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796560/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Andrew H -- Valdez, Gregorio -- Moresi, Viviana -- Qi, Xiaoxia -- McAnally, John -- Elliott, Jeffrey L -- Bassel-Duby, Rhonda -- Sanes, Joshua R -- Olson, Eric N -- 1F32NS061464-01A1/NS/NINDS NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1/HL/NHLBI NIH HHS/ -- T32HL007360/HL/NHLBI NIH HHS/ -- U24 CA126608/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1549-54. doi: 10.1126/science.1181046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007902" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Axons/physiology ; Carrier Proteins/genetics/metabolism ; Disease Models, Animal ; Disease Progression ; Fibroblast Growth Factors/metabolism ; Histone Deacetylases/genetics/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Motor Neurons/pathology/*physiology ; Muscle Denervation ; Muscle, Skeletal/innervation/*metabolism/pathology ; MyoD Protein/genetics/metabolism ; Myogenin/genetics/metabolism ; Nerve Regeneration ; Neuromuscular Junction/growth & development/*pathology/*physiology ; RNA Interference ; Signal Transduction ; Transcriptional Activation ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 57
    facet.materialart.
    Unknown
    Trapping moving targets with small molecules (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: Structure-based drug design traditionally uses static protein models as inspirations for focusing on "active" site targets. Allosteric regulation of biological macromolecules, however, is affected by both conformational and dynamic properties of the protein or protein complex and can potentially lead to more avenues for therapeutic development. We discuss the advantages of searching for molecules that conformationally trap a macromolecule in its inactive state. Although multiple methodologies exist to probe protein dynamics and ligand binding, our current discussion highlights the use of nuclear magnetic resonance spectroscopy in the drug discovery and design process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981433/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Gregory M -- Craik, Charles S -- 1R01A1067423/PHS HHS/ -- P30-AI027763/AI/NIAID NIH HHS/ -- P50 GM082250/GM/NIGMS NIH HHS/ -- P50 GM082250-02/GM/NIGMS NIH HHS/ -- R01 AI067423/AI/NIAID NIH HHS/ -- R01 AI067423-01A1/AI/NIAID NIH HHS/ -- R01 AI067423-02/AI/NIAID NIH HHS/ -- R01 AI067423-03/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):213-5. doi: 10.1126/science.1169378.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmaceutical Chemistry, University of California, San Francisco (UCSF), 600 16th Street, Box 2280, San Francisco, CA 94158-2280, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359579" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Allosteric Site ; Apoproteins/chemistry/metabolism ; Benzamides ; CREB-Binding Protein/chemistry/metabolism ; Catalytic Domain ; Cyclic AMP Response Element-Binding Protein/chemistry/metabolism ; *Drug Design ; *Drug Discovery ; Enzyme Inhibitors/chemistry/pharmacology ; Imatinib Mesylate ; Ligands ; Nuclear Magnetic Resonance, Biomolecular ; Piperazines/metabolism/pharmacology ; Protein Binding ; *Protein Conformation ; Protein Multimerization ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Proteins/antagonists & inhibitors/*chemistry/metabolism ; Proto-Oncogene Proteins c-mdm2/chemistry/metabolism ; Pyrimidines/metabolism/pharmacology ; Signal Transduction ; Small Molecule Libraries ; Thermodynamics ; Tumor Suppressor Protein p53/chemistry/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 58
    facet.materialart.
    Unknown
    AMPK regulates the circadian clock by cryptochrome phosphorylation and degradation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Circadian clocks coordinate behavioral and physiological processes with daily light-dark cycles by driving rhythmic transcription of thousands of genes. Whereas the master clock in the brain is set by light, pacemakers in peripheral organs, such as the liver, are reset by food availability, although the setting, or "entrainment," mechanisms remain mysterious. Studying mouse fibroblasts, we demonstrated that the nutrient-responsive adenosine monophosphate-activated protein kinase (AMPK) phosphorylates and destabilizes the clock component cryptochrome 1 (CRY1). In mouse livers, AMPK activity and nuclear localization were rhythmic and inversely correlated with CRY1 nuclear protein abundance. Stimulation of AMPK destabilized cryptochromes and altered circadian rhythms, and mice in which the AMPK pathway was genetically disrupted showed alterations in peripheral clocks. Thus, phosphorylation by AMPK enables cryptochrome to transduce nutrient signals to circadian clocks in mammalian peripheral organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Sachdeva, Uma M -- DiTacchio, Luciano -- Williams, Elliot C -- Alvarez, Jacqueline G -- Egan, Daniel F -- Vasquez, Debbie S -- Juguilon, Henry -- Panda, Satchidananda -- Shaw, Reuben J -- Thompson, Craig B -- Evans, Ronald M -- CA104838/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK080425/DK/NIDDK NIH HHS/ -- EY016807/EY/NEI NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- P01 CA104838-05S1/CA/NCI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-03/DK/NIDDK NIH HHS/ -- R01 EY016807/EY/NEI NIH HHS/ -- R01 EY016807-03/EY/NEI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-31/DK/NIDDK NIH HHS/ -- T32 HL007439/HL/NHLBI NIH HHS/ -- T32 HL007439-27/HL/NHLBI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-08S19002/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):437-40. doi: 10.1126/science.1172156.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, the Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833968" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; ARNTL Transcription Factors ; Amino Acid Substitution ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Circadian Rhythm/*physiology ; Cryptochromes ; Culture Media ; Flavoproteins/genetics/*metabolism ; Food ; Glucose/metabolism/pharmacology ; Humans ; Liver/*metabolism ; Mice ; Mutagenesis, Site-Directed ; Mutant Proteins/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Stability ; Recombinant Fusion Proteins/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 59
    facet.materialart.
    Unknown
    Development. Aorta's cardinal secret (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benedito, Rui -- Adams, Ralf H -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):242-3. doi: 10.1126/science.1181033.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, 48149 Munster, Germany, and Faculty of Medicine, University of Munster, 48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/cytology/*embryology ; Arteries/cytology/*embryology ; Blood Circulation ; Cell Movement ; Endothelial Cells/cytology/metabolism/*physiology ; Ephrin-B2/metabolism ; Lymphatic Vessels/embryology ; Mice ; *Morphogenesis ; Neovascularization, Physiologic ; Receptor, EphB4/metabolism ; Signal Transduction ; Stem Cells/cytology/physiology ; Veins/cytology/*embryology ; Zebrafish ; Zebrafish Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 60
    facet.materialart.
    Unknown
    Competitive interactions between cells: death, growth, and geography (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: Competitive interactions between cells are the basis of many homeostatic processes in biology. Some of the best-described cases of competition between cells occur in Drosophila: cell competition, whereby somatic cells within a growing epithelium compete with one another for contribution to the adult, and stem cell competition, in which germline or somatic stem cells vie for residency in the niche. Both types of competition are conserved physiological processes, with much to tell us about how cellular neighborhoods influence cell behavior, and have importance to stem cell biology, regeneration and transplantation, and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736143/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736143/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnston, Laura A -- GMO78464/PHS HHS/ -- HD42770/HD/NICHD NIH HHS/ -- R01 GM078464/GM/NIGMS NIH HHS/ -- R01 GM078464-01/GM/NIGMS NIH HHS/ -- R01 GM078464-02/GM/NIGMS NIH HHS/ -- R01 GM078464-03/GM/NIGMS NIH HHS/ -- R01 HD042770/HD/NICHD NIH HHS/ -- R01 HD042770-02/HD/NICHD NIH HHS/ -- R01 HD042770-03/HD/NICHD NIH HHS/ -- R01 HD042770-04/HD/NICHD NIH HHS/ -- R01 HD042770-05/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1679-82. doi: 10.1126/science.1163862.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. lj180@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; *Cell Communication ; *Cell Physiological Phenomena ; *Cell Proliferation ; Drosophila/cytology ; Homeostasis ; Models, Biological ; Signal Transduction ; Stem Cell Niche/physiology ; Stem Cells/cytology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 61
    facet.materialart.
    Unknown
    Neuroscience. Brain wiring by presorting axons (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyamichi, Kazunari -- Luo, Liqun -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):544-5. doi: 10.1126/science.1178117.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644096" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Brain Mapping ; Cell Communication ; Cyclic AMP/metabolism ; Mice ; Neuroglia/physiology ; Neuropilin-1/metabolism ; Olfactory Bulb/cytology/*physiology ; Olfactory Mucosa/cytology/physiology ; Olfactory Pathways/cytology/*physiology ; Olfactory Receptor Neurons/cytology/*physiology ; Receptors, Odorant/metabolism ; Semaphorin-3A/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 62
    facet.materialart.
    Unknown
    Deletion of Atoh1 disrupts Sonic Hedgehog signaling in the developing cerebellum and prevents medulloblastoma (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Granule neuron precursors (GNPs) are the most actively proliferating cells in the postnatal nervous system, and mutations in pathways that control the GNP cell cycle can result in medulloblastoma. The transcription factor Atoh1 has been suspected to contribute to GNP proliferation, but its role in normal and neoplastic postnatal cerebellar development remains unexplored. We show that Atoh1 regulates the signal transduction pathway of Sonic Hedgehog, an extracellular factor that is essential for GNP proliferation, and demonstrate that deletion of Atoh1 prevents cerebellar neoplasia in a mouse model of medulloblastoma. Our data shed light on the function of Atoh1 in postnatal cerebellar development and identify a new mechanism that can be targeted to regulate medulloblastoma formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638077/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638077/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flora, Adriano -- Klisch, Tiemo J -- Schuster, Gabriele -- Zoghbi, Huda Y -- 5 P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1424-7. doi: 10.1126/science.1181453.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*genetics/*physiology ; Cell Cycle ; Cell Differentiation ; Cell Proliferation ; Cerebellar Neoplasms/etiology/*prevention & control ; Cerebellum/cytology/growth & development/*metabolism ; Down-Regulation ; Gene Deletion ; Gene Knock-In Techniques ; Hedgehog Proteins/*metabolism ; Kruppel-Like Transcription Factors/genetics/metabolism ; Medulloblastoma/etiology/*prevention & control ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Neurons/*cytology ; Receptors, G-Protein-Coupled/genetics/physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 63
    facet.materialart.
    Unknown
    A G protein-coupled receptor is essential for Schwann cells to initiate myelination (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-12
    Description: The myelin sheath allows axons to conduct action potentials rapidly in the vertebrate nervous system. Axonal signals activate expression of specific transcription factors, including Oct6 and Krox20, that initiate myelination in Schwann cells. Elevation of cyclic adenosine monophosphate (cAMP) can mimic axonal contact in vitro, but the mechanisms that regulate cAMP levels in vivo are unknown. Using mutational analysis in zebrafish, we found that the G protein-coupled receptor Gpr126 is required autonomously in Schwann cells for myelination. In gpr126 mutants, Schwann cells failed to express oct6 and krox20 and were arrested at the promyelinating stage. Elevation of cAMP in gpr126 mutants, but not krox20 mutants, could restore myelination. We propose that Gpr126 drives the differentiation of promyelinating Schwann cells by elevating cAMP levels, thereby triggering Oct6 expression and myelination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856697/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856697/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monk, Kelly R -- Naylor, Stephen G -- Glenn, Thomas D -- Mercurio, Sara -- Perlin, Julie R -- Dominguez, Claudia -- Moens, Cecilia B -- Talbot, William S -- GFP03011/Telethon/Italy -- HG002995/HG/NHGRI NIH HHS/ -- R01 NS050223/NS/NINDS NIH HHS/ -- R01 NS050223-04/NS/NINDS NIH HHS/ -- R56 NS050223/NS/NINDS NIH HHS/ -- R56 NS050223-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Sep 11;325(5946):1402-5. doi: 10.1126/science.1173474.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19745155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology/ultrastructure ; Cell Differentiation ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Early Growth Response Protein 2/genetics/metabolism ; Embryo, Nonmammalian/cytology/metabolism ; Lateral Line System/innervation ; Molecular Sequence Data ; Mutation ; Myelin Basic Protein/metabolism ; Myelin Sheath/*physiology ; Neuregulin-1/metabolism ; Octamer Transcription Factor-6/genetics/metabolism ; Receptor, ErbB-3/genetics/metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Schwann Cells/cytology/*metabolism ; Signal Transduction ; Zebrafish/embryology/genetics/growth & development/*metabolism ; Zebrafish Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 64
    facet.materialart.
    Unknown
    Nuclear hormone receptor regulation of microRNAs controls developmental progression (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: In response to small-molecule signals such as retinoids or steroids, nuclear receptors activate gene expression to regulate development in different tissues. MicroRNAs turn off target gene expression within cells by binding complementary regions in messenger RNA transcripts, and they have been broadly implicated in development and disease. Here we show that the Caenorhabditis elegans nuclear receptor DAF-12 and its steroidal ligand directly activate promoters of let-7 microRNA family members to down-regulate the microRNA target hbl-1, which drives progression of epidermal stem cells from second to third larval stage patterns of cell division. Conversely, the receptor without the ligand represses microRNA expression during developmental arrest. These findings identify microRNAs as components of a hormone-coupled molecular switch that shuts off earlier developmental programs to allow for later ones.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757405/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757405/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bethke, Axel -- Fielenbach, Nicole -- Wang, Zhu -- Mangelsdorf, David J -- Antebi, Adam -- GM077201/GM/NIGMS NIH HHS/ -- R01 GM077201/GM/NIGMS NIH HHS/ -- R01 GM077201-03/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):95-8. doi: 10.1126/science.1164899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Huffington Center on Aging, Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/cytology/genetics/*growth & development/*metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Line ; Cholestenes/*metabolism ; DNA-Binding Proteins/genetics/metabolism ; Down-Regulation ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Humans ; Ligands ; MicroRNAs/*genetics ; Mutation ; RNA, Helminth/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*metabolism ; Response Elements ; Signal Transduction ; Transcription Factors/genetics/metabolism ; Transfection ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 65
    facet.materialart.
    Unknown
    Halofuginone inhibits TH17 cell differentiation by activating the amino acid starvation response (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: A central challenge for improving autoimmune therapy is preventing inflammatory pathology without inducing generalized immunosuppression. T helper 17 (TH17) cells, characterized by their production of interleukin-17, have emerged as important and broad mediators of autoimmunity. Here we show that the small molecule halofuginone (HF) selectively inhibits mouse and human TH17 differentiation by activating a cytoprotective signaling pathway, the amino acid starvation response (AAR). Inhibition of TH17 differentiation by HF is rescued by the addition of excess amino acids and is mimicked by AAR activation after selective amino acid depletion. HF also induces the AAR in vivo and protects mice from TH17-associated experimental autoimmune encephalomyelitis. These results indicate that the AAR pathway is a potent and selective regulator of inflammatory T cell differentiation in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803727/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803727/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sundrud, Mark S -- Koralov, Sergei B -- Feuerer, Markus -- Calado, Dinis Pedro -- Kozhaya, Aimee Elhed -- Rhule-Smith, Ava -- Lefebvre, Rachel E -- Unutmaz, Derya -- Mazitschek, Ralph -- Waldner, Hanspeter -- Whitman, Malcolm -- Keller, Tracy -- Rao, Anjana -- R01 AI040127/AI/NIAID NIH HHS/ -- R01 AI040127-09/AI/NIAID NIH HHS/ -- R01 AI048213/AI/NIAID NIH HHS/ -- R01 AI048213-01/AI/NIAID NIH HHS/ -- R01 CA042471/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1334-8. doi: 10.1126/science.1172638.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School and Immune Disease Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498172" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 4/metabolism ; Amino Acids/*metabolism/pharmacology ; Animals ; Autoimmunity/drug effects ; Cell Differentiation/drug effects ; Cytokines/metabolism ; Encephalomyelitis, Autoimmune, Experimental/drug therapy/immunology ; Eukaryotic Initiation Factor-2/metabolism ; Gene Expression ; Humans ; Interleukin-17/biosynthesis/genetics ; Lymphopoiesis/drug effects ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Piperidines/*pharmacology/therapeutic use ; Protein-Serine-Threonine Kinases/metabolism ; Quinazolinones/*pharmacology/therapeutic use ; Signal Transduction ; T-Lymphocyte Subsets/cytology/*drug effects/immunology/metabolism ; T-Lymphocytes, Helper-Inducer/cytology/*drug effects/immunology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 66
    facet.materialart.
    Unknown
    Cell biology. Moonlighting in mitochondria (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, Martin G Jr -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):723-4. doi: 10.1126/science.1169660.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Metabolism, Endocrinology and Diabetes, Department of Internal Medicine, and Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA. mgmyers@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19197047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Cell Respiration ; Cytokines/metabolism ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Mice ; Mitochondria/*metabolism ; Mitochondria, Heart/metabolism ; Mitochondria, Liver/metabolism ; *Oxidative Phosphorylation ; Phosphorylation ; STAT3 Transcription Factor/chemistry/*metabolism ; Serine/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 67
    facet.materialart.
    Unknown
    Cytosolic viral sensor RIG-I is a 5'-triphosphate-dependent translocase on double-stranded RNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-03
    Description: Retinoic acid inducible-gene I (RIG-I) is a cytosolic multidomain protein that detects viral RNA and elicits an antiviral immune response. Two N-terminal caspase activation and recruitment domains (CARDs) transmit the signal, and the regulatory domain prevents signaling in the absence of viral RNA. 5'-triphosphate and double-stranded RNA (dsRNA) are two molecular patterns that enable RIG-I to discriminate pathogenic from self-RNA. However, the function of the DExH box helicase domain that is also required for activity is less clear. Using single-molecule protein-induced fluorescence enhancement, we discovered a robust adenosine 5'-triphosphate-powered dsRNA translocation activity of RIG-I. The CARDs dramatically suppress translocation in the absence of 5'-triphosphate, and the activation by 5'-triphosphate triggers RIG-I to translocate preferentially on dsRNA in cis. This functional integration of two RNA molecular patterns may provide a means to specifically sense and counteract replicating viruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567915/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567915/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myong, Sua -- Cui, Sheng -- Cornish, Peter V -- Kirchhofer, Axel -- Gack, Michaela U -- Jung, Jae U -- Hopfner, Karl-Peter -- Ha, Taekjip -- CA82057/CA/NCI NIH HHS/ -- R01 GM065367/GM/NIGMS NIH HHS/ -- R01-GM065367/GM/NIGMS NIH HHS/ -- U19 AI083025/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1070-4. doi: 10.1126/science.1168352. Epub 2009 Jan 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 West Gregory Drive, Champaign, IL 61801, USA. smyong@uiuc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119185" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Cell Line ; Cytosol/metabolism ; DEAD-box RNA Helicases/chemistry/genetics/*metabolism ; Kinetics ; Nucleic Acid Heteroduplexes ; Protein Structure, Tertiary ; RNA/metabolism ; RNA, Double-Stranded/*metabolism ; RNA, Viral/metabolism ; Receptors, Pattern Recognition/chemistry/genetics/*metabolism ; Signal Transduction ; Temperature
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 68
    facet.materialart.
    Unknown
    Host inhibition of a bacterial virulence effector triggers immunity to infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-09
    Description: Plant pathogenic bacteria secrete effector proteins that attack the host signaling machinery to suppress immunity. Effectors can be recognized by hosts leading to immunity. One such effector is AvrPtoB of Pseudomonas syringae, which degrades host protein kinases, such as tomato Fen, through an E3 ligase domain. Pto kinase, which is highly related to Fen, recognizes AvrPtoB in conjunction with the resistance protein Prf. Here we show that Pto is resistant to AvrPtoB-mediated degradation because it inactivates the E3 ligase domain. AvrPtoB ubiquitinated Fen within the catalytic cleft, leading to its breakdown and loss of the associated Prf protein. Pto avoids this by phosphorylating and inactivating the AvrPtoB E3 domain. Thus, inactivation of a pathogen virulence molecule is one mechanism by which plants resist disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ntoukakis, Vardis -- Mucyn, Tatiana S -- Gimenez-Ibanez, Selena -- Chapman, Helen C -- Gutierrez, Jose R -- Balmuth, Alexi L -- Jones, Alexandra M E -- Rathjen, John P -- BB/D00456X/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 May 8;324(5928):784-7. doi: 10.1126/science.1169430.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sainsbury Laboratory, Colney, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423826" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Immunity, Innate ; Lycopersicon esculentum/genetics/*metabolism/*microbiology ; Mutant Proteins/metabolism ; Phosphorylation ; Plant Diseases/immunology/*microbiology ; Plant Leaves/metabolism ; Plant Proteins/*metabolism ; Plants, Genetically Modified ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*metabolism ; Pseudomonas syringae/genetics/growth & development/metabolism/*pathogenicity ; Signal Transduction ; Tobacco/genetics/metabolism/microbiology ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Virulence Factors/antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 69
    facet.materialart.
    Unknown
    Developmental biology. Strategies to get arrested (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Akira -- Sommer, Ralf J -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):944-5. doi: 10.1126/science.1183272.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Developmental Biology, 72076 Tubingen, Germany. akira.ogawa@tuebingen.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/*growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/*physiology ; Cues ; Genes, Helminth ; Longevity ; Mutation ; Pheromones/physiology ; Receptors, Cytoplasmic and Nuclear/genetics/physiology ; Receptors, G-Protein-Coupled/genetics/physiology ; Reproduction ; Signal Transduction ; Stress, Physiological
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 70
    facet.materialart.
    Unknown
    The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: Deposition of the amyloid-beta peptide is a pathological hallmark of Alzheimer's disease. A high-throughput functional genomics screen identified G protein-coupled receptor 3 (GPR3), a constitutively active orphan G protein-coupled receptor, as a modulator of amyloid-beta production. Overexpression of GPR3 stimulated amyloid-beta production, whereas genetic ablation of GPR3 prevented accumulation of the amyloid-beta peptide in vitro and in an Alzheimer's disease mouse model. GPR3 expression led to increased formation and cell-surface localization of the mature gamma-secretase complex in the absence of an effect on Notch processing. GPR3 is highly expressed in areas of the normal human brain implicated in Alzheimer's disease and is elevated in the sporadic Alzheimer's disease brain. Thus, GPR3 represents a potential therapeutic target for the treatment of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thathiah, Amantha -- Spittaels, Kurt -- Hoffmann, Marcel -- Staes, Mik -- Cohen, Adrian -- Horre, Katrien -- Vanbrabant, Mieke -- Coun, Frea -- Baekelandt, Veerle -- Delacourte, Andre -- Fischer, David F -- Pollet, Dirk -- De Strooper, Bart -- Merchiers, Pascal -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):946-51. doi: 10.1126/science.1160649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Developmental Genetics, Vlaams Institute for Biotechnology, Center for Human Genetics, Catholic University of Leuven, Herestraat 49, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213921" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Female ; Humans ; Male ; Mice ; Middle Aged ; Neurons/*metabolism ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/*metabolism ; Receptors, Notch/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 71
    facet.materialart.
    Unknown
    Cell biology. Two lipids that give direction (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887428/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cote, Jean-Francois -- Vuori, Kristiina -- 77591/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):346-7. doi: 10.1126/science.1173646.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Recherches Cliniques de Montreal, Universite de Montreal, Montreal, Quebec H2W 1R7, Canada. jean-francois.cote@ircm.qc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; Cell Polarity ; *Chemotaxis, Leukocyte ; Feedback, Physiological ; GTPase-Activating Proteins/genetics/*metabolism ; Mice ; Neutrophils/cytology/*physiology ; Phosphatidic Acids/*metabolism ; Phosphatidylinositol Phosphates/*metabolism ; Pseudopodia/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 72
    facet.materialart.
    Unknown
    Sequential regulation of DOCK2 dynamics by two phospholipids during neutrophil chemotaxis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: During chemotaxis, activation of the small guanosine triphosphatase Rac is spatially regulated to organize the extension of membrane protrusions in the direction of migration. In neutrophils, Rac activation is primarily mediated by DOCK2, an atypical guanine nucleotide exchange factor. Upon stimulation, we found that DOCK2 rapidly translocated to the plasma membrane in a phosphatidylinositol 3,4,5-trisphosphate-dependent manner. However, subsequent accumulation of DOCK2 at the leading edge required phospholipase D-mediated synthesis of phosphatidic acid, which stabilized DOCK2 there by means of interaction with a polybasic amino acid cluster, resulting in increased local actin polymerization. When this interaction was blocked, neutrophils failed to form leading edges properly and exhibited defects in chemotaxis. Thus, intracellular DOCK2 dynamics are sequentially regulated by distinct phospholipids to localize Rac activation during neutrophil chemotaxis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3761877/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3761877/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishikimi, Akihiko -- Fukuhara, Hideo -- Su, Wenjuan -- Hongu, Tsunaki -- Takasuga, Shunsuke -- Mihara, Hisashi -- Cao, Qinhong -- Sanematsu, Fumiyuki -- Kanai, Motomu -- Hasegawa, Hiroshi -- Tanaka, Yoshihiko -- Shibasaki, Masakatsu -- Kanaho, Yasunori -- Sasaki, Takehiko -- Frohman, Michael A -- Fukui, Yoshinori -- R01 GM084251/GM/NIGMS NIH HHS/ -- R01GM71520/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):384-7. doi: 10.1126/science.1170179. Epub 2009 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325080" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Butanol/pharmacology ; Actins/metabolism ; Animals ; Cell Line ; Cell Membrane/*metabolism ; Cell Polarity ; *Chemotaxis, Leukocyte ; Enzyme Inhibitors/pharmacology ; GTPase-Activating Proteins/chemistry/genetics/*metabolism ; Humans ; Mice ; Neutrophils/cytology/drug effects/*physiology ; Phosphatidic Acids/*metabolism/pharmacology ; Phosphatidylinositol Phosphates/*metabolism ; Phospholipase D/genetics/metabolism ; Protein Binding ; Pseudopodia/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 73
    facet.materialart.
    Unknown
    Mitochondrial STAT3 supports Ras-dependent oncogenic transformation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: Signal transducer and activator of transcription 3 (STAT3) is a latent cytoplasmic transcription factor responsive to cytokine signaling and tyrosine kinase oncoproteins by nuclear translocation when it is tyrosine-phosphorylated. We report that malignant transformation by activated Ras is impaired without STAT3, in spite of the inability of Ras to drive STAT3 tyrosine phosphorylation or nuclear translocation. Moreover, STAT3 mutants that cannot be tyrosine-phosphorylated, that are retained in the cytoplasm, or that cannot bind DNA nonetheless supported Ras-mediated transformation. Unexpectedly, STAT3 was detected within mitochondria, and exclusive targeting of STAT3 to mitochondria without nuclear accumulation facilitated Ras transformation. Mitochondrial STAT3 sustained altered glycolytic and oxidative phosphorylation activities characteristic of cancer cells. Thus, in addition to its nuclear transcriptional role, STAT3 regulates a metabolic function in mitochondria, supporting Ras-dependent malignant transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840701/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840701/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gough, Daniel J -- Corlett, Alicia -- Schlessinger, Karni -- Wegrzyn, Joanna -- Larner, Andrew C -- Levy, David E -- R01 AI028900/AI/NIAID NIH HHS/ -- R01 AI028900-19/AI/NIAID NIH HHS/ -- R01AI28900/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1713-6. doi: 10.1126/science.1171721.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and New York University Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation ; Cell Survival ; *Cell Transformation, Neoplastic ; Genes, ras ; Glycolysis ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred BALB C ; Mitochondria/*metabolism ; Mutant Proteins/metabolism ; Neoplasms, Experimental/metabolism/pathology ; Neoplastic Stem Cells ; Oxidative Phosphorylation ; Phosphorylation ; STAT3 Transcription Factor/genetics/*metabolism ; Signal Transduction ; ras Proteins/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 74
    facet.materialart.
    Unknown
    Genome-wide RNAi screen identifies genes involved in intestinal pathogenic bacterial infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-13
    Description: Innate immunity represents the first line of defense in animals. We report a genome-wide in vivo Drosophila RNA interference screen to uncover genes involved in susceptibility or resistance to intestinal infection with the bacterium Serratia marcescens. We first employed whole-organism gene suppression, followed by tissue-specific silencing in gut epithelium or hemocytes to identify several hundred genes involved in intestinal antibacterial immunity. Among the pathways identified, we showed that the JAK-STAT signaling pathway controls host defense in the gut by regulating stem cell proliferation and thus epithelial cell homeostasis. Therefore, we revealed multiple genes involved in antibacterial defense and the regulation of innate immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975362/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975362/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cronin, Shane J F -- Nehme, Nadine T -- Limmer, Stefanie -- Liegeois, Samuel -- Pospisilik, J Andrew -- Schramek, Daniel -- Leibbrandt, Andreas -- Simoes, Ricardo de Matos -- Gruber, Susanne -- Puc, Urszula -- Ebersberger, Ingo -- Zoranovic, Tamara -- Neely, G Gregory -- von Haeseler, Arndt -- Ferrandon, Dominique -- Penninger, Josef M -- P01 AI044220/AI/NIAID NIH HHS/ -- P01 AI044220-10/AI/NIAID NIH HHS/ -- P01 AI44220/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):340-3. doi: 10.1126/science.1173164. Epub 2009 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, A-1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19520911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Proliferation ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/*genetics/immunology/*microbiology ; Epithelial Cells/cytology/physiology ; *Genome, Insect ; Hemocytes/immunology/metabolism/microbiology ; Homeostasis ; Immunity, Innate/*genetics ; Intestinal Mucosa/cytology/immunology/metabolism/microbiology ; Janus Kinases/genetics/metabolism ; Models, Animal ; *RNA Interference ; STAT Transcription Factors/genetics/metabolism ; Serratia Infections/genetics/*immunology/microbiology ; Serratia marcescens/*immunology/physiology ; Signal Transduction ; Stem Cells/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 75
    facet.materialart.
    Unknown
    Understanding the Warburg effect: the metabolic requirements of cell proliferation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-23
    Description: In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5'-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849637/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vander Heiden, Matthew G -- Cantley, Lewis C -- Thompson, Craig B -- R01 CA092660/CA/NCI NIH HHS/ -- R01 CA092660-09/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- R01 CA105463-06/CA/NCI NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1029-33. doi: 10.1126/science.1160809.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19460998" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Aerobiosis ; Amino Acids/biosynthesis ; Animals ; *Cell Proliferation ; Glucose/metabolism ; *Glycolysis ; Humans ; Lipids/biosynthesis ; Metabolic Networks and Pathways ; Mutation ; Neoplasms/genetics/*metabolism/*pathology ; Nucleotides/biosynthesis ; Oxidative Phosphorylation ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 76
    facet.materialart.
    Unknown
    Functional proteomics identify cornichon proteins as auxiliary subunits of AMPA receptors (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-07
    Description: Glutamate receptors of the AMPA-subtype (AMPARs), together with the transmembrane AMPAR regulatory proteins (TARPs), mediate fast excitatory synaptic transmission in the mammalian brain. Here, we show by proteomic analysis that the majority of AMPARs in the rat brain are coassembled with two members of the cornichon family of transmembrane proteins, rather than with the TARPs. Coassembly with cornichon homologs 2 and 3 affects AMPARs in two ways: Cornichons increase surface expression of AMPARs, and they alter channel gating by markedly slowing deactivation and desensitization kinetics. These results demonstrate that cornichons are intrinsic auxiliary subunits of native AMPARs and provide previously unknown molecular determinants for glutamatergic neurotransmission in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwenk, Jochen -- Harmel, Nadine -- Zolles, Gerd -- Bildl, Wolfgang -- Kulik, Akos -- Heimrich, Bernd -- Chisaka, Osamu -- Jonas, Peter -- Schulte, Uwe -- Fakler, Bernd -- Klocker, Nikolaj -- New York, N.Y. -- Science. 2009 Mar 6;323(5919):1313-9. doi: 10.1126/science.1167852.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology II, University of Freiburg, Engesserstrasse 4, 79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19265014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/*metabolism ; Cell Membrane/metabolism ; Glutamic Acid/metabolism ; Immunohistochemistry ; *Ion Channel Gating ; Kinetics ; Membrane Proteins/chemistry/metabolism ; Mice ; Neurons/*metabolism ; Patch-Clamp Techniques ; Protein Subunits/chemistry/metabolism ; Proteomics ; Rats ; Receptors, AMPA/chemistry/*metabolism ; Signal Transduction ; Synapses/metabolism ; *Synaptic Transmission ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 77
    facet.materialart.
    Unknown
    Viral glycosphingolipids induce lytic infection and cell death in marine phytoplankton (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-07
    Description: Marine viruses that infect phytoplankton are recognized as a major ecological and evolutionary driving force, shaping community structure and nutrient cycling in the marine environment. Little is known about the signal transduction pathways mediating viral infection. We show that viral glycosphingolipids regulate infection of Emiliania huxleyi, a cosmopolitan coccolithophore that plays a major role in the global carbon cycle. These sphingolipids derive from an unprecedented cluster of biosynthetic genes in Coccolithovirus genomes, are synthesized de novo during lytic infection, and are enriched in virion membranes. Purified glycosphingolipids induced biochemical hallmarks of programmed cell death in an uninfected host. These lipids were detected in coccolithophore populations in the North Atlantic, which highlights their potential as biomarkers for viral infection in the oceans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vardi, Assaf -- Van Mooy, Benjamin A S -- Fredricks, Helen F -- Popendorf, Kimberly J -- Ossolinski, Justin E -- Haramaty, Liti -- Bidle, Kay D -- New York, N.Y. -- Science. 2009 Nov 6;326(5954):861-5. doi: 10.1126/science.1177322.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Environmental Biophysics and Molecular Ecology Group, Institute of Marine and Coastal Sciences, Rutgers University, 71 Dudley Road, New Brunswick, NJ 08901, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892986" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Atlantic Ocean ; Biomarkers/analysis ; Caspases/metabolism ; Cell Membrane/chemistry ; Cell Proliferation ; Gene Expression ; Genes, Viral ; Glycosphingolipids/analysis/biosynthesis/*physiology ; Host-Pathogen Interactions ; Photosynthesis ; Phycodnaviridae/genetics/isolation & purification/*physiology ; Phytoplankton/chemistry/cytology/*physiology/*virology ; *Seawater/chemistry/virology ; Signal Transduction ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 78
    facet.materialart.
    Unknown
    Cell biology. Sorting out diabetes (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orme, Charisse M -- Bogan, Jonathan S -- New York, N.Y. -- Science. 2009 May 29;324(5931):1155-6. doi: 10.1126/science.1174841.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8020, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478173" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism/ultrastructure ; Animals ; Blood Glucose/metabolism ; Cell Membrane/metabolism ; Clathrin/*metabolism ; Clathrin Heavy Chains ; Clathrin-Coated Vesicles/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Glucose/*metabolism ; Glucose Transporter Type 4/*metabolism ; Humans ; Insulin/blood ; Mice ; Muscle Cells/*metabolism/ultrastructure ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 79
    facet.materialart.
    Unknown
    Auxin-dependent patterning and gamete specification in the Arabidopsis female gametophyte (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: The female reproductive unit of flowering plants, the haploid female gametophyte, is highly reduced relative to other land plants. We show that patterning of the Arabidopsis female gametophyte depends on an asymmetric distribution of the hormone auxin during its syncitial development. Furthermore, this auxin gradient is correlated with location-specific auxin biosynthesis, rather than auxin efflux that directs patterning in the diploid sporophytic tissues comprising the rest of the plant. Manipulation of auxin responses or synthesis induces switching of gametic and nongametic cell identities and specialized nonreproductive cells to exhibit attributes presumptively lost during angiosperm evolution. These findings may account for the unique egg cell specification characteristic of angiosperms and the formation of seeds with single diploid embryos while containing endosperm that can have variable numbers of parental haploid genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pagnussat, Gabriela C -- Alandete-Saez, Monica -- Bowman, John L -- Sundaresan, Venkatesan -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1684-9. doi: 10.1126/science.1167324. Epub 2009 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498110" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*cytology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/genetics/metabolism ; Biological Evolution ; Down-Regulation ; Flowers/*cytology/growth & development/metabolism ; Gene Expression Regulation, Plant ; Genes, Plant ; Germ Cells/*cytology/growth & development/metabolism ; Indoleacetic Acids/*metabolism ; Membrane Transport Proteins/genetics/metabolism ; MicroRNAs ; Mitosis ; Models, Biological ; Oxygenases/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Seeds/cytology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 80
    facet.materialart.
    Unknown
    Patterning mechanisms of branched organs (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Branching morphogenesis is one of the earliest events essential for the success of metazoans. By branching out and forming cellular or tissue extensions, cells can maximize their surface area and overcome space constraints posed by organ size. Over the past decade, tremendous progress has been made toward understanding the branching mechanisms of various invertebrate and vertebrate organ systems. Despite their distinct origins, morphologies and functions, different cell and tissue types use a remarkably conserved set of tools to undergo branching morphogenesis. Recent studies have shed important light on the basis of molecular conservation in the formation of branched structures in diverse organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645229/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Pengfei -- Werb, Zena -- CA057621/CA/NCI NIH HHS/ -- ES012801/ES/NIEHS NIH HHS/ -- R01 CA057621/CA/NCI NIH HHS/ -- R01 CA057621-16A1/CA/NCI NIH HHS/ -- U01 ES012801-06/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1506-9. doi: 10.1126/science.1162783.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Program in Developmental Biology, University of California at San Francisco, San Francisco, CA 94143-0452, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/embryology/physiology ; *Body Patterning ; Cell Differentiation ; Epithelium/embryology/physiology ; Genes ; Mesoderm/embryology/physiology ; *Morphogenesis ; Nervous System/embryology ; Neurons/cytology ; *Organogenesis ; Regeneration ; Signal Transduction ; Stem Cells/physiology ; Stromal Cells/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 81
    facet.materialart.
    Unknown
    Comment on "Genetically determined differences in learning from errors" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-16
    Description: Klein et al. (Reports, 7 December 2007, p. 1642) used individuals with a polymorphism adjacent to the dopamine receptor 2 gene as naturally occurring models for reduced brain dopamine receptor density in a probabilistic learning task. We raise the concern that this polymorphism resides in the gene for the kinase ANKK1, where it causes a nonconservative amino acid exchange.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lucht, Michael -- Rosskopf, Dieter -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):200; author reply 200. doi: 10.1126/science.1155372.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital for Psychiatry and Psychotherapy, Haus 30, Ernst-Moritz-Arndt University, Greifswald, Stralsund 18437, Germany. lucht@uni-greifswald.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18621654" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Brain/metabolism ; Cloning, Molecular ; Humans ; *Learning ; *Polymorphism, Genetic ; Protein-Serine-Threonine Kinases/*genetics/physiology ; Proteins/genetics/physiology ; Receptors, Dopamine D2/*genetics/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 82
    facet.materialart.
    Unknown
    Systems biology. Enlightening Rhythms (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipan, Ovidiu -- New York, N.Y. -- Science. 2008 Jan 25;319(5862):417-8. doi: 10.1126/science.1154208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of Richmond, Richmond, VA 23173, USA. olipan@richmond.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18218882" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; *Feedback, Physiological ; Gene Regulatory Networks ; Glycerol/*metabolism ; Mitogen-Activated Protein Kinases/genetics/metabolism ; *Models, Biological ; Osmolar Concentration ; Osmotic Pressure ; Saccharomyces cerevisiae/genetics/metabolism/*physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Signal Transduction ; Systems Biology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 83
    facet.materialart.
    Unknown
    Tight regulation of unstructured proteins: from transcript synthesis to protein degradation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Altered abundance of several intrinsically unstructured proteins (IUPs) has been associated with perturbed cellular signaling that may lead to pathological conditions such as cancer. Therefore, it is important to understand how cells precisely regulate the availability of IUPs. We observed that regulation of transcript clearance, proteolytic degradation, and translational rate contribute to controlling the abundance of IUPs, some of which are present in low amounts and for short periods of time. Abundant phosphorylation and low stochasticity in transcription and translation indicate that the availability of IUPs can be finely tuned. Fidelity in signaling may require that most IUPs be available in appropriate amounts and not present longer than needed.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803065/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803065/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gsponer, Jorg -- Futschik, Matthias E -- Teichmann, Sarah A -- Babu, M Madan -- G0600158/Medical Research Council/United Kingdom -- MC_U105161047/Medical Research Council/United Kingdom -- MC_U105185859/Medical Research Council/United Kingdom -- U.1051.04.027.00001.01 (85859)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1365-8. doi: 10.1126/science.1163581.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK. jgsponer@mrc-lmb.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039133" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Cycle ; Computational Biology ; Genes, Fungal ; Humans ; Phosphorylation ; Protein Biosynthesis ; Protein Conformation ; Protein Kinases/metabolism ; Proteome/chemistry ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Saccharomyces cerevisiae/chemistry/cytology/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/*chemistry/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/chemistry/metabolism ; Signal Transduction ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 84
    facet.materialart.
    Unknown
    The premetazoan ancestry of cadherins (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: Cadherin-mediated cell adhesion and signaling is essential for metazoan development and yet is absent from all other multicellular organisms. We found cadherin genes at numbers similar to those observed in complex metazoans in one of the closest single-celled relatives of metazoans, the choanoflagellate Monosiga brevicollis. Because the evolution of metazoans from a single-celled ancestor required novel cell adhesion and signaling mechanisms, the discovery of diverse cadherins in choanoflagellates suggests that cadherins may have contributed to metazoan origins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abedin, Monika -- King, Nicole -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):946-8. doi: 10.1126/science.1151084.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology and Center for Integrative Genomics, University of California at Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276888" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Amino Acid Sequence ; Animals ; Base Sequence ; *Biological Evolution ; Cadherins/*chemistry/*genetics/physiology ; Cell Adhesion ; Ciona intestinalis/chemistry ; Cnidaria/chemistry ; Drosophila melanogaster/chemistry ; Eukaryota/*chemistry ; Eukaryotic Cells/*chemistry/physiology ; Mice ; Molecular Sequence Data ; Protein Structure, Tertiary ; Repetitive Sequences, Amino Acid ; Signal Transduction ; Tyrosine/metabolism ; src Homology Domains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 85
    facet.materialart.
    Unknown
    A genetic framework for the control of cell division and differentiation in the root meristem (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Plant growth and development are sustained by meristems. Meristem activity is controlled by auxin and cytokinin, two hormones whose interactions in determining a specific developmental output are still poorly understood. By means of a comprehensive genetic and molecular analysis in Arabidopsis, we show that a primary cytokinin-response transcription factor, ARR1, activates the gene SHY2/IAA3 (SHY2), a repressor of auxin signaling that negatively regulates the PIN auxin transport facilitator genes: thereby, cytokinin causes auxin redistribution, prompting cell differentiation. Conversely, auxin mediates degradation of the SHY2 protein, sustaining PIN activities and cell division. Thus, the cell differentiation and division balance necessary for controlling root meristem size and root growth is the result of the interaction between cytokinin and auxin through a simple regulatory circuit converging on the SHY2 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dello Ioio, Raffaele -- Nakamura, Kinu -- Moubayidin, Laila -- Perilli, Serena -- Taniguchi, Masatoshi -- Morita, Miyo T -- Aoyama, Takashi -- Costantino, Paolo -- Sabatini, Sabrina -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1380-4. doi: 10.1126/science.1164147.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartimento di Genetica e Biologia Molecolare, Laboratorio di Genomica e Proteomica Funzionale dei Sistemi Modello (FGPL), Universita La Sapienza - Piazzale Aldo Moro 5, 00185 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039136" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*cytology/genetics/growth & development/metabolism ; Arabidopsis Proteins/*genetics/*metabolism ; Cell Differentiation ; Cell Division ; Cytokinins/genetics/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation, Plant ; Genes, Plant ; Indoleacetic Acids/*metabolism ; Membrane Transport Proteins/genetics/metabolism ; Meristem/*cytology/growth & development ; Nuclear Proteins/*genetics/metabolism ; Plant Roots/*cytology/growth & development ; Promoter Regions, Genetic ; Signal Transduction ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 86
    facet.materialart.
    Unknown
    Neuroscience. Rules of plasticity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brecht, Michael -- Schmitz, Dietmar -- New York, N.Y. -- Science. 2008 Jan 4;319(5859):39-40. doi: 10.1126/science.1153231.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bernstein Center for Computational Neuroscience, Humboldt-University Berlin, 10115 Berlin, Germany. michael.brecht@bccn-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174422" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association Learning ; Calcium/metabolism ; Long-Term Potentiation ; Memory ; Mice ; *Neuronal Plasticity ; Neurons/physiology ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Signal Transduction ; Somatosensory Cortex/cytology/*physiology ; Synapses/*physiology ; Synaptic Membranes/metabolism ; Vibrissae/innervation/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 87
    facet.materialart.
    Unknown
    Hepatic glucose sensing via the CREB coactivator CRTC2 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: Chronic hyperglycemia contributes to the development of diabetes-associated complications. Increases in the concentration of circulating glucose activate the hexosamine biosynthetic pathway (HBP) and promote the O-glycosylation of proteins by O-glycosyl transferase (OGT). We show that OGT triggered hepatic gluconeogenesis through the O-glycosylation of the transducer of regulated cyclic adenosine monophosphate response element-binding protein (CREB) 2 (TORC2 or CRTC2). CRTC2 was O-glycosylated at sites that normally sequester CRTC2 in the cytoplasm through a phosphorylation-dependent mechanism. Decreasing amounts of O-glycosylated CRTC2 by expression of the deglycosylating enzyme O-GlcNAcase blocked effects of glucose on gluconeogenesis, demonstrating the importance of the HBP in the development of glucose intolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dentin, Renaud -- Hedrick, Susan -- Xie, Jianxin -- Yates, John 3rd -- Montminy, Marc -- R01 GM037828/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1402-5. doi: 10.1126/science.1151363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323454" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Diabetes Mellitus/metabolism ; *Gluconeogenesis ; Glucose/*metabolism ; Glycosylation ; Glycosyltransferases/metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; RNA Interference ; Signal Transduction ; Trans-Activators/genetics/*metabolism ; Transcription Factors ; beta-N-Acetylhexosaminidases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 88
    facet.materialart.
    Unknown
    An agonist of toll-like receptor 5 has radioprotective activity in mouse and primate models (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: The toxicity of ionizing radiation is associated with massive apoptosis in radiosensitive organs. Here, we investigate whether a drug that activates a signaling mechanism used by tumor cells to suppress apoptosis can protect healthy cells from the harmful effects of radiation. We studied CBLB502, a polypeptide drug derived from Salmonella flagellin that binds to Toll-like receptor 5 (TLR5) and activates nuclear factor-kappaB signaling. A single injection of CBLB502 before lethal total-body irradiation protected mice from both gastrointestinal and hematopoietic acute radiation syndromes and resulted in improved survival. CBLB502 injected after irradiation also enhanced survival, but at lower radiation doses. It is noteworthy that the drug did not decrease tumor radiosensitivity in mouse models. CBLB502 also showed radioprotective activity in lethally irradiated rhesus monkeys. Thus, TLR5 agonists could potentially improve the therapeutic index of cancer radiotherapy and serve as biological protectants in radiation emergencies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322935/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burdelya, Lyudmila G -- Krivokrysenko, Vadim I -- Tallant, Thomas C -- Strom, Evguenia -- Gleiberman, Anatoly S -- Gupta, Damodar -- Kurnasov, Oleg V -- Fort, Farrel L -- Osterman, Andrei L -- Didonato, Joseph A -- Feinstein, Elena -- Gudkov, Andrei V -- AI066497/AI/NIAID NIH HHS/ -- CA75179/CA/NCI NIH HHS/ -- CA84406/CA/NCI NIH HHS/ -- R01 CA084406/CA/NCI NIH HHS/ -- R01 CA084406-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):226-30. doi: 10.1126/science.1154986.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403709" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/drug effects/radiation effects ; Chemotherapy, Adjuvant ; Flagellin/chemistry/pharmacology ; Gamma Rays ; Hematopoietic System/drug effects/radiation effects ; Intestine, Small/cytology/drug effects/radiation effects ; Macaca mulatta ; Mice ; Mice, Inbred ICR ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Neoplasms, Experimental/drug therapy/radiotherapy ; Peptides/administration & dosage/chemistry/*pharmacology/toxicity ; Radiation Dosage ; Radiation Injuries, Experimental/*prevention & control ; Radiation Tolerance/*drug effects ; Radiation-Protective Agents/administration & ; dosage/chemistry/*pharmacology/toxicity ; Salmonella enterica ; Signal Transduction ; Toll-Like Receptor 5/*agonists/metabolism ; Whole-Body Irradiation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 89
    facet.materialart.
    Unknown
    A model for neuronal competition during development (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its own receptor TrkA in mouse and rat neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain-derived neurotrophic factor and neurotrophin-4, which, through the receptor p75, can kill neighboring neurons with low retrograde NGF-TrkA signaling whereas neurons with high NGF-TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deppmann, Christopher D -- Mihalas, Stefan -- Sharma, Nikhil -- Lonze, Bonnie E -- Niebur, Ernst -- Ginty, David D -- EY016281/EY/NEI NIH HHS/ -- F32 NS053187/NS/NINDS NIH HHS/ -- NS053187/NS/NINDS NIH HHS/ -- NS34814/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):369-73. doi: 10.1126/science.1152677. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Apoptosis ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Survival ; Cells, Cultured ; Computer Simulation ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Mathematics ; Mice ; *Models, Neurological ; Nerve Growth Factor/*metabolism ; Nerve Growth Factors/metabolism ; Neurons/cytology/*physiology ; Oligonucleotide Array Sequence Analysis ; Rats ; Receptor, trkA/genetics/*metabolism ; Receptors, Nerve Growth Factor/genetics/metabolism ; Signal Transduction ; Superior Cervical Ganglion/*cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 90
    facet.materialart.
    Unknown
    Comment on "Brain IRS2 signaling coordinates life span and nutrient homeostasis" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: Taguchi et al. (Reports, 20 July 2007, p. 369) reported that mice heterozygous for a null mutation in insulin receptor substrate-2 (Irs2) display a 17% increase in median life span. However, using the same mouse model, we find no evidence for life-span extension and suggest that the findings of Taguchi et al. were due to atypical life-span profiles in their study animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selman, Colin -- Lingard, Steven -- Gems, David -- Partridge, Linda -- Withers, Dominic J -- New York, N.Y. -- Science. 2008 May 23;320(5879):1012; author reply 1012. doi: 10.1126/science.1152366.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Diabetes and Endocrinology, Department of Medicine, University College London, Rayne Institute, 5 University Street, London WC1E 6JJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Crosses, Genetic ; Diet ; Female ; Homeostasis ; Insulin Receptor Substrate Proteins ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Kaplan-Meier Estimate ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phosphoproteins/genetics/*metabolism ; Research Design ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 91
    facet.materialart.
    Unknown
    An integrated genomic analysis of human glioblastoma multiforme (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. To identify the genetic alterations in GBMs, we sequenced 20,661 protein coding genes, determined the presence of amplifications and deletions using high-density oligonucleotide arrays, and performed gene expression analyses using next-generation sequencing technologies in 22 human tumor samples. This comprehensive analysis led to the discovery of a variety of genes that were not known to be altered in GBMs. Most notably, we found recurrent mutations in the active site of isocitrate dehydrogenase 1 (IDH1) in 12% of GBM patients. Mutations in IDH1 occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival. These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Jones, Sian -- Zhang, Xiaosong -- Lin, Jimmy Cheng-Ho -- Leary, Rebecca J -- Angenendt, Philipp -- Mankoo, Parminder -- Carter, Hannah -- Siu, I-Mei -- Gallia, Gary L -- Olivi, Alessandro -- McLendon, Roger -- Rasheed, B Ahmed -- Keir, Stephen -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Busam, Dana A -- Tekleab, Hanna -- Diaz, Luis A Jr -- Hartigan, James -- Smith, Doug R -- Strausberg, Robert L -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Yan, Hai -- Riggins, Gregory J -- Bigner, Darell D -- Karchin, Rachel -- Papadopoulos, Nick -- Parmigiani, Giovanni -- Vogelstein, Bert -- Velculescu, Victor E -- Kinzler, Kenneth W -- 5P50-NS-20023/NS/NINDS NIH HHS/ -- CA09547/CA/NCI NIH HHS/ -- CA108786/CA/NCI NIH HHS/ -- CA11898/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- NS052507/NS/NINDS NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-160017/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R01 CA140316/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-27/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-13/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1807-12. doi: 10.1126/science.1164382. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics, and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772396" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/*genetics/mortality ; Female ; Gene Amplification ; Gene Dosage ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genome, Human ; Glioblastoma/*genetics/mortality ; Humans ; Isocitrate Dehydrogenase/chemistry/*genetics ; Male ; Middle Aged ; *Mutation ; Mutation, Missense ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Signal Transduction ; Survival Rate
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 92
    facet.materialart.
    Unknown
    Pyogenic bacterial infections in humans with MyD88 deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bernuth, Horst -- Picard, Capucine -- Jin, Zhongbo -- Pankla, Rungnapa -- Xiao, Hui -- Ku, Cheng-Lung -- Chrabieh, Maya -- Mustapha, Imen Ben -- Ghandil, Pegah -- Camcioglu, Yildiz -- Vasconcelos, Julia -- Sirvent, Nicolas -- Guedes, Margarida -- Vitor, Artur Bonito -- Herrero-Mata, Maria Jose -- Arostegui, Juan Ignacio -- Rodrigo, Carlos -- Alsina, Laia -- Ruiz-Ortiz, Estibaliz -- Juan, Manel -- Fortuny, Claudia -- Yague, Jordi -- Anton, Jordi -- Pascal, Mariona -- Chang, Huey-Hsuan -- Janniere, Lucile -- Rose, Yoann -- Garty, Ben-Zion -- Chapel, Helen -- Issekutz, Andrew -- Marodi, Laszlo -- Rodriguez-Gallego, Carlos -- Banchereau, Jacques -- Abel, Laurent -- Li, Xiaoxia -- Chaussabel, Damien -- Puel, Anne -- Casanova, Jean-Laurent -- U19 AI057234/AI/NIAID NIH HHS/ -- U19 AI057234-02/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):691-6. doi: 10.1126/science.1158298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, INSERM U550, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669862" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Bacterial Infections/*genetics/*immunology ; Cell Line, Transformed ; Child ; Child, Preschool ; Cytokines/metabolism ; Disease Susceptibility ; Female ; Gene Deletion ; Humans ; Immunity, Innate ; Male ; Mice ; Mutation, Missense ; Myeloid Differentiation Factor 88/*deficiency/genetics/metabolism ; Pneumococcal Infections/genetics/immunology ; Pseudomonas Infections/genetics/immunology ; Receptors, Interleukin-1/immunology/metabolism ; Signal Transduction ; Staphylococcal Infections/genetics/immunology ; Toll-Like Receptors/immunology/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 93
    facet.materialart.
    Unknown
    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 94
    facet.materialart.
    Unknown
    The serine protease TMPRSS6 is required to sense iron deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Hepcidin, a liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron content. Several proteins induce expression of the hepcidin-encoding gene Hamp in response to infection or high levels of iron. However, mechanism(s) of Hamp suppression during iron depletion are poorly understood. We describe mask: a recessive, chemically induced mutant mouse phenotype, characterized by progressive loss of body (but not facial) hair and microcytic anemia. The mask phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is due to a splicing defect in the transmembrane serine protease 6 gene Tmprss6. Overexpression of normal TMPRSS6 protein suppresses activation of the Hamp promoter, and the TMPRSS6 cytoplasmic domain mediates Hamp suppression via proximal promoter element(s). TMPRSS6 is an essential component of a pathway that detects iron deficiency and blocks Hamp transcription, permitting enhanced dietary iron absorption.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430097/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Xin -- She, Ellen -- Gelbart, Terri -- Truksa, Jaroslav -- Lee, Pauline -- Xia, Yu -- Khovananth, Kevin -- Mudd, Suzanne -- Mann, Navjiwan -- Moresco, Eva Marie Y -- Beutler, Ernest -- Beutler, Bruce -- AI054523/AI/NIAID NIH HHS/ -- DK53505-09/DK/NIDDK NIH HHS/ -- R01 DK053505-09/DK/NIDDK NIH HHS/ -- U54 AI054523/AI/NIAID NIH HHS/ -- U54 AI054523-019005/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1088-92. doi: 10.1126/science.1157121. Epub 2008 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451267" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Macrocytic/genetics/metabolism ; Animals ; Antimicrobial Cationic Peptides/*genetics/metabolism ; Cell Line, Tumor ; Gene Expression Regulation ; Hepcidins ; Humans ; Iron/blood/*deficiency/metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Biological ; Mutation ; Phenotype ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Serine Endopeptidases/chemistry/genetics/*metabolism ; Signal Transduction ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 95
    facet.materialart.
    Unknown
    Dichotomous dopaminergic control of striatal synaptic plasticity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-09
    Description: At synapses between cortical pyramidal neurons and principal striatal medium spiny neurons (MSNs), postsynaptic D1 and D2 dopamine (DA) receptors are postulated to be necessary for the induction of long-term potentiation and depression, respectively-forms of plasticity thought to underlie associative learning. Because these receptors are restricted to two distinct MSN populations, this postulate demands that synaptic plasticity be unidirectional in each cell type. Using brain slices from DA receptor transgenic mice, we show that this is not the case. Rather, DA plays complementary roles in these two types of MSN to ensure that synaptic plasticity is bidirectional and Hebbian. In models of Parkinson's disease, this system is thrown out of balance, leading to unidirectional changes in plasticity that could underlie network pathology and symptoms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833421/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833421/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Weixing -- Flajolet, Marc -- Greengard, Paul -- Surmeier, D James -- DA10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- NS 34696/NS/NINDS NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-05/MH/NIMH NIH HHS/ -- R01 NS034696/NS/NINDS NIH HHS/ -- R01 NS034696-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 8;321(5890):848-51. doi: 10.1126/science.1160575.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18687967" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cannabinoid Receptor Modulators/metabolism ; Corpus Striatum/cytology/*physiology ; Dopamine/*physiology ; Glutamic Acid/metabolism ; *Long-Term Potentiation ; *Long-Term Synaptic Depression ; Mice ; Mice, Transgenic ; Neurons/*physiology ; Parkinsonian Disorders/*physiopathology ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; Signal Transduction ; Synapses/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 96
    facet.materialart.
    Unknown
    Inhibition of Rac by the GAP activity of centralspindlin is essential for cytokinesis (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: During cytokinesis, the guanosine triphosphatase (GTPase) RhoA orchestrates contractile ring assembly and constriction. RhoA signaling is controlled by the central spindle, a set of microtubule bundles that forms between the separating chromosomes. Centralspindlin, a protein complex consisting of the kinesin-6 ZEN-4 and the Rho family GTPase activating protein (GAP) CYK-4, is required for central spindle assembly and cytokinesis in Caenorhabditis elegans. However, the importance of the CYK-4 GAP activity and whether it regulates RhoA remain unclear. We found that two separation-of-function mutations in the GAP domain of CYK-4 lead to cytokinesis defects that mimic centralspindlin loss of function. These defects could be rescued by depletion of the GTPase Rac or its effectors, but not by depletion of RhoA. Thus, inactivation of Rac by centralspindlin functions in parallel with RhoA activation to drive contractile ring constriction during cytokinesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736296/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736296/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canman, Julie C -- Lewellyn, Lindsay -- Laband, Kimberley -- Smerdon, Stephen J -- Desai, Arshad -- Bowerman, Bruce -- Oegema, Karen -- GM058017/GM/NIGMS NIH HHS/ -- MC_U117584228/Medical Research Council/United Kingdom -- R01 GM049869/GM/NIGMS NIH HHS/ -- R01 GM049869-15/GM/NIGMS NIH HHS/ -- R01 GM058017/GM/NIGMS NIH HHS/ -- T32 CA067754/CA/NCI NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1543-6. doi: 10.1126/science.1163086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Biology, University of Oregon, Eugene, OR 97403, USA. jcanman@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056985" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Caenorhabditis elegans/*cytology/embryology/genetics/*metabolism ; Caenorhabditis elegans Proteins/*antagonists & ; inhibitors/chemistry/genetics/*metabolism ; *Cytokinesis ; Embryo, Nonmammalian/cytology/metabolism ; GTPase-Activating Proteins/chemistry/genetics/metabolism ; Genes, Helminth ; Kinesin/metabolism ; Mutation ; Protein Structure, Tertiary ; Signal Transduction ; Spindle Apparatus/physiology/ultrastructure ; rac GTP-Binding Proteins/*antagonists & inhibitors/metabolism ; rhoA GTP-Binding Protein/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 97
    facet.materialart.
    Unknown
    Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-29
    Description: Schizophrenia is a devastating neurodevelopmental disorder whose genetic influences remain elusive. We hypothesize that individually rare structural variants contribute to the illness. Microdeletions and microduplications 〉100 kilobases were identified by microarray comparative genomic hybridization of genomic DNA from 150 individuals with schizophrenia and 268 ancestry-matched controls. All variants were validated by high-resolution platforms. Novel deletions and duplications of genes were present in 5% of controls versus 15% of cases and 20% of young-onset cases, both highly significant differences. The association was independently replicated in patients with childhood-onset schizophrenia as compared with their parents. Mutations in cases disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways. These results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, Tom -- McClellan, Jon M -- McCarthy, Shane E -- Addington, Anjene M -- Pierce, Sarah B -- Cooper, Greg M -- Nord, Alex S -- Kusenda, Mary -- Malhotra, Dheeraj -- Bhandari, Abhishek -- Stray, Sunday M -- Rippey, Caitlin F -- Roccanova, Patricia -- Makarov, Vlad -- Lakshmi, B -- Findling, Robert L -- Sikich, Linmarie -- Stromberg, Thomas -- Merriman, Barry -- Gogtay, Nitin -- Butler, Philip -- Eckstrand, Kristen -- Noory, Laila -- Gochman, Peter -- Long, Robert -- Chen, Zugen -- Davis, Sean -- Baker, Carl -- Eichler, Evan E -- Meltzer, Paul S -- Nelson, Stanley F -- Singleton, Andrew B -- Lee, Ming K -- Rapoport, Judith L -- King, Mary-Claire -- Sebat, Jonathan -- HD043569/HD/NICHD NIH HHS/ -- M01 RR000046/RR/NCRR NIH HHS/ -- MH061355/MH/NIMH NIH HHS/ -- MH061464/MH/NIMH NIH HHS/ -- MH061528/MH/NIMH NIH HHS/ -- NS052108/NS/NINDS NIH HHS/ -- R01 HD043569/HD/NICHD NIH HHS/ -- RR000046/RR/NCRR NIH HHS/ -- RR025014/RR/NCRR NIH HHS/ -- U01 MH061355/MH/NIMH NIH HHS/ -- U01 MH061464/MH/NIMH NIH HHS/ -- U01 MH061528/MH/NIMH NIH HHS/ -- U24 NS052108/NS/NINDS NIH HHS/ -- UL1 RR025014/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):539-43. doi: 10.1126/science.1155174. Epub 2008 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369103" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age of Onset ; Amino Acid Sequence ; Brain/cytology/*growth & development/metabolism ; Case-Control Studies ; Child ; Excitatory Amino Acid Transporter 1/chemistry/genetics/physiology ; Female ; *Gene Deletion ; *Gene Duplication ; Genetic Predisposition to Disease ; Genome, Human ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neurons/cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Receptor, Epidermal Growth Factor/chemistry/genetics/physiology ; Receptor, ErbB-4 ; Schizophrenia/*genetics/physiopathology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 98
    facet.materialart.
    Unknown
    Identification of SLEEPLESS, a sleep-promoting factor (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-19
    Description: Sleep is an essential process conserved from flies to humans. The importance of sleep is underscored by its tight homeostatic control. Through a forward genetic screen, we identified a gene, sleepless, required for sleep in Drosophila. The sleepless gene encodes a brain-enriched, glycosylphosphatidylinositol-anchored protein. Loss of SLEEPLESS protein caused an extreme (〉80%) reduction in sleep; a moderate reduction in SLEEPLESS had minimal effects on baseline sleep but markedly reduced the amount of recovery sleep after sleep deprivation. Genetic and molecular analyses revealed that quiver, a mutation that impairs Shaker-dependent potassium current, is an allele of sleepless. Consistent with this finding, Shaker protein levels were reduced in sleepless mutants. We propose that SLEEPLESS is a signaling molecule that connects sleep drive to lowered membrane excitability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771549/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771549/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, Kyunghee -- Joiner, William J -- Wu, Mark N -- Yue, Zhifeng -- Smith, Corinne J -- Sehgal, Amita -- AG017628/AG/NIA NIH HHS/ -- P01 AG017628/AG/NIA NIH HHS/ -- P01 AG017628-070004/AG/NIA NIH HHS/ -- R01 NS072431/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):372-6. doi: 10.1126/science.1155942.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635795" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Behavior, Animal ; Brain/metabolism ; Cell Membrane/metabolism ; DNA Transposable Elements ; Drosophila Proteins/chemistry/*genetics/*physiology ; Drosophila melanogaster/genetics/*physiology ; Female ; *Genes, Insect ; Glycosylphosphatidylinositols ; Homeostasis ; Longevity ; Male ; Membrane Proteins/chemistry/*genetics/*physiology ; *Models, Animal ; Molecular Sequence Data ; Mutation ; Phenotype ; Shaker Superfamily of Potassium Channels/physiology ; Signal Transduction ; *Sleep/genetics/physiology ; Sleep Deprivation ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 99
    facet.materialart.
    Unknown
    Developmental biology. Aging of the ovary linked to PTEN pathway (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):558-9. doi: 10.1126/science.319.5863.558b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239099" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Female ; Forkhead Transcription Factors/genetics/physiology ; Humans ; Mice ; Oocytes/*physiology ; Ovarian Follicle/*physiology ; Ovulation ; PTEN Phosphohydrolase/antagonists & inhibitors/genetics/*physiology ; Primary Ovarian Insufficiency/*physiopathology/therapy ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 100
    facet.materialart.
    Unknown
    Beta-arrestin-mediated localization of smoothened to the primary cilium (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: beta-Arrestins have important roles in the regulation of seven-transmembrane receptors (7TMRs). Smoothened (Smo) is a 7TMR that mediates effects of Hedgehog on developmental processes and whose dysregulation may cause tumorigenesis. beta-Arrestins are required for endocytosis of Smo and signaling to Gli transcription factors. In mammalian cells, Smo-dependent signaling requires translocation to primary cilia. We demonstrated that beta-arrestins mediate the activity-dependent interaction of Smo and the kinesin motor protein Kif3A. This multimeric complex localized to primary cilia and was disrupted in cells transfected with beta-arrestin small interfering RNA. beta-Arrestin 1 or beta-arrestin 2 depletion prevented the localization of Smo to primary cilia and the Smo-dependent activation of Gli. These results suggest roles for beta-arrestins in mediating the intracellular transport of a 7TMR to its obligate subcellular location for signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587210/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovacs, Jeffrey J -- Whalen, Erin J -- Liu, Renshui -- Xiao, Kunhong -- Kim, Jihee -- Chen, Minyong -- Wang, Jiangbo -- Chen, Wei -- Lefkowitz, Robert J -- 5R01 CA113656-02/CA/NCI NIH HHS/ -- 5T32 AI007217-25/AI/NIAID NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- HL70631/HL/NHLBI NIH HHS/ -- R01 CA113656/CA/NCI NIH HHS/ -- R01 CA113656-02/CA/NCI NIH HHS/ -- R01 CA113656-03/CA/NCI NIH HHS/ -- R01 HL016037/HL/NHLBI NIH HHS/ -- R01 HL016037-35/HL/NHLBI NIH HHS/ -- R01 HL070631/HL/NHLBI NIH HHS/ -- R01 HL070631-04/HL/NHLBI NIH HHS/ -- T32 AI007217/AI/NIAID NIH HHS/ -- T32 AI007217-25/AI/NIAID NIH HHS/ -- T32 AI007217-26/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1777-81. doi: 10.1126/science.1157983. Epub 2008 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*metabolism ; Cilia/*metabolism ; Hedgehog Proteins/metabolism ; Kinesin/*metabolism ; Mice ; Microscopy, Confocal ; Molecular Motor Proteins/*metabolism ; NIH 3T3 Cells ; Protein Transport ; RNA Interference ; Receptors, G-Protein-Coupled/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...