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  • Signal Transduction  (57)
  • American Association for the Advancement of Science (AAAS)  (57)
  • American Society of Hematology
  • EMBO Press
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • 2005-2009  (57)
  • 2006  (57)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (57)
  • American Society of Hematology
  • EMBO Press
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
Years
  • 2005-2009  (57)
Year
  • 1
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    Lhx2 maintains stem cell character in hair follicles (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: During embryogenesis, stem cells are set aside to fuel the postnatal hair cycle and repair the epidermis after injury. To define how hair follicle stem cells are specified and maintained in an undifferentiated state, we developed a strategy to isolate and transcriptionally profile embryonic hair progenitors in mice. We identified Lhx2 as a transcription factor positioned downstream of signals necessary to specify hair follicle stem cells, but upstream from signals required to drive activated stem cells to terminally differentiate. Using gain- and loss-of-function studies, we uncovered a role for Lhx2 in maintaining the growth and undifferentiated properties of hair follicle progenitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2405918/" 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/PMC2405918/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhee, Horace -- Polak, Lisa -- Fuchs, Elaine -- R01 AR031737/AR/NIAMS NIH HHS/ -- R01 AR031737-24/AR/NIAMS NIH HHS/ -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01 AR050452-04/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rockefeller University, 1230 York Avenue, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Epidermis/cytology/embryology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Hair/embryology/growth & development ; Hair Follicle/*cytology/embryology/physiology ; Homeodomain Proteins/genetics/*physiology ; LIM-Homeodomain Proteins ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Morphogenesis ; Oligonucleotide Array Sequence Analysis ; Signal Transduction ; Skin Transplantation ; Stem Cells/*physiology ; 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
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  • 2
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    Immunology. Restless T cells sniff and go (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustelin, Tomas -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1902-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program on Inflammatory Disease Research, Infectious and Inflammatory Disease Center, and Program of Signal Transduction, Cancer Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA. tmustelin@burnham.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD ; Antigens, CD28/metabolism ; Antigens, CD80/metabolism ; Antigens, CD86/metabolism ; Antigens, Differentiation/genetics/*physiology ; *Autoimmunity ; CTLA-4 Antigen ; Cell Adhesion ; Cell Movement ; Dendritic Cells/immunology ; Humans ; Integrins/physiology ; Ligands ; Lymph Nodes/*immunology ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Cell signaling. A new way to burn fat (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neels, Jaap G -- Olefsky, Jerrold M -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1756-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0673, USA. jolefsky@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794069" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl-CoA Carboxylase/antagonists & inhibitors/*metabolism ; Adipocytes/metabolism ; Adipose Tissue/*metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Energy Intake ; Energy Metabolism ; Enzyme Activation ; Fasting ; Fatty Acids/metabolism ; Hepatocytes/metabolism ; Insulin/physiology ; Insulin Resistance ; *Lipid Metabolism ; Lipogenesis ; Liver/metabolism ; Malonyl Coenzyme A/metabolism ; Mice ; Models, Biological ; Nuclear Proteins/*metabolism ; Obesity/therapy ; Oxidation-Reduction ; Phosphorylation ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cell biology. Purinergic chemotaxis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linden, Joel -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA. jlinden@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170280" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Adenosine Monophosphate/metabolism ; Adenosine Triphosphate/*metabolism ; Animals ; Apyrase/pharmacology ; *Autocrine Communication ; Blood Platelets/metabolism ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Endothelial Cells/metabolism ; Mice ; Models, Biological ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophils/drug effects/*metabolism/physiology ; Receptor, Adenosine A3/metabolism ; Receptors, Purinergic/*metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y2 ; Respiratory Burst/drug effects ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482474/" 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/PMC1482474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Judge, Daniel P -- Holm, Tammy M -- Cohn, Ronald D -- Loeys, Bart L -- Cooper, Timothy K -- Myers, Loretha -- Klein, Erin C -- Liu, Guosheng -- Calvi, Carla -- Podowski, Megan -- Neptune, Enid R -- Halushka, Marc K -- Bedja, Djahida -- Gabrielson, Kathleen -- Rifkin, Daniel B -- Carta, Luca -- Ramirez, Francesco -- Huso, David L -- Dietz, Harry C -- K08 HL067056/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pediatrics, 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/16601194" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Antagonists/administration & dosage/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/administration & dosage/*therapeutic use ; Animals ; Antibodies/immunology ; Aorta/pathology ; Aortic Aneurysm/etiology/*prevention & control ; *Disease Models, Animal ; Elastic Tissue/pathology ; Female ; Losartan/administration & dosage/*therapeutic use ; Lung/pathology ; Lung Diseases/drug therapy/pathology ; Marfan Syndrome/complications/*drug therapy/metabolism/pathology ; Mice ; Microfilament Proteins/genetics ; Mutation ; Neutralization Tests ; Pregnancy ; Pregnancy Complications/drug therapy ; Propranolol/administration & dosage/therapeutic use ; Pulmonary Alveoli/pathology ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Neuroscience. Neuron, know thy neighbor (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiCicco-Bloom, Emanuel -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1560-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Cell Biology/Pediatrics (Neurology), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA. diciccem@umdnj.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543446" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Animals ; Brain/cytology/*embryology ; *Cell Adhesion ; Cell Count ; Cell Death ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Central Nervous System/cytology/embryology ; Cytoskeleton/physiology ; Hedgehog Proteins ; Hyperplasia ; Mice ; Mutation ; Neurons/cytology/*physiology ; Signal Transduction ; Stem Cells/cytology/physiology ; Trans-Activators/*metabolism ; alpha Catenin/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    ATP release guides neutrophil chemotaxis via P2Y2 and A3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: Cells must amplify external signals to orient and migrate in chemotactic gradient fields. We find that human neutrophils release adenosine triphosphate (ATP) from the leading edge of the cell surface to amplify chemotactic signals and direct cell orientation by feedback through P2Y2 nucleotide receptors. Neutrophils rapidly hydrolyze released ATP to adenosine that then acts via A3-type adenosine receptors, which are recruited to the leading edge, to promote cell migration. Thus, ATP release and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling gradient sensing and migration of neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Yu -- Corriden, Ross -- Inoue, Yoshiaki -- Yip, Linda -- Hashiguchi, Naoyuki -- Zinkernagel, Annelies -- Nizet, Victor -- Insel, Paul A -- Junger, Wolfgang G -- GM-60475/GM/NIGMS NIH HHS/ -- GM-66232/GM/NIGMS NIH HHS/ -- PR043034/PR/OCPHP CDC HHS/ -- R01 GM-51477/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of California San Diego, San Diego, CA 92103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170310" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism/pharmacology ; Adenosine A3 Receptor Agonists ; Adenosine A3 Receptor Antagonists ; Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacology ; Animals ; *Autocrine Communication ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Cytoplasmic Granules/metabolism ; HL-60 Cells ; Humans ; Hydrolysis ; Mice ; Mice, Knockout ; Neutrophils/drug effects/metabolism/*physiology ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A3/*metabolism ; Receptors, Purinergic P2/*metabolism ; Receptors, Purinergic P2Y2 ; Signal Transduction ; Suramin/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Lamin A-dependent nuclear defects in human aging (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: Mutations in the nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HGPS). Whether lamin A plays any role in normal aging is unknown. We show that the same molecular mechanism responsible for HGPS is active in healthy cells. Cell nuclei from old individuals acquire defects similar to those of HGPS patient cells, including changes in histone modifications and increased DNA damage. Age-related nuclear defects are caused by sporadic use, in healthy individuals, of the same cryptic splice site in lamin A whose constitutive activation causes HGPS. Inhibition of this splice site reverses the nuclear defects associated with aging. These observations implicate lamin A in physiological aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1855250/" 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/PMC1855250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scaffidi, Paola -- Misteli, Tom -- Z01 BC010309-07/BC/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 May 19;312(5776):1059-63. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645051" target="_blank"〉PubMed〈/a〉
    Keywords: Aged, 80 and over ; Aging/*physiology ; Cell Line ; Cell Nucleus/pathology ; DNA Damage ; Exons ; Histones/metabolism ; Humans ; Lamin Type A/genetics/*physiology ; Progeria/genetics/pathology ; RNA Splicing/genetics ; Signal Transduction ; Tumor Suppressor Protein p53/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-21
    Description: The tumor suppressor programmed cell death protein 4 (PDCD4) inhibits the translation initiation factor eIF4A, an RNA helicase that catalyzes the unwinding of secondary structure at the 5' untranslated region (5'UTR) of messenger RNAs (mRNAs). In response to mitogens, PDCD4 was rapidly phosphorylated on Ser67 by the protein kinase S6K1 and subsequently degraded via the ubiquitin ligase SCF(betaTRCP). Expression in cultured cells of a stable PDCD4 mutant that is unable to bind betaTRCP inhibited translation of an mRNA with a structured 5'UTR, resulted in smaller cell size, and slowed down cell cycle progression. We propose that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis and consequently cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorrello, N Valerio -- Peschiaroli, Angelo -- Guardavaccaro, Daniele -- Colburn, Nancy H -- Sherman, Nicholas E -- Pagano, Michele -- R01-CA76584/CA/NCI NIH HHS/ -- R01-GM57587/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):467-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053147" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Amino Acid Motifs ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Size ; Eukaryotic Initiation Factor-4A/antagonists & inhibitors/metabolism ; Eukaryotic Initiation Factor-4F/metabolism ; Eukaryotic Initiation Factor-4G/metabolism ; Eukaryotic Initiation Factors/metabolism ; Humans ; Mitogens/pharmacology ; Phosphorylation ; *Protein Biosynthesis ; RNA, Small Interfering ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Ribosomal Protein S6 Kinases/metabolism ; SKP Cullin F-Box Protein Ligases/*metabolism ; Serine/metabolism ; Serum ; Signal Transduction ; beta-Transducin Repeat-Containing Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
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  • 10
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    A critical role for the innate immune signaling molecule IRAK-4 in T cell activation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: IRAK-4 is a protein kinase that is pivotal in mediating signals for innate immune responses. Here, we report that IRAK-4 signaling is also essential for eliciting adaptive immune responses. Thus, in the absence of IRAK-4, in vivo T cell responses were significantly impaired. Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase C activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor kappaB. Our findings suggest that T cells use this critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Nobutaka -- Suzuki, Shinobu -- Millar, Douglas G -- Unno, Midori -- Hara, Hiromitsu -- Calzascia, Thomas -- Yamasaki, Sho -- Yokosuka, Tadashi -- Chen, Nien-Jung -- Elford, Alisha R -- Suzuki, Jun-Ichiro -- Takeuchi, Arata -- Mirtsos, Christine -- Bouchard, Denis -- Ohashi, Pamela S -- Yeh, Wen-Chen -- Saito, Takashi -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1927-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama City, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574867" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Activation ; Immunity, Innate ; Interleukin-1 Receptor-Associated Kinases ; Isoenzymes/metabolism ; *Lymphocyte Activation ; Membrane Microdomains/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; ZAP-70 Protein-Tyrosine Kinase/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Alterations in 5-HT1B receptor function by p11 in depression-like states (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: The pathophysiology of depression remains enigmatic, although abnormalities in serotonin signaling have been implicated. We have found that the serotonin 1B receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11. p11 increases localization of 5-HT1B receptors at the cell surface. p11 is increased in rodent brains by antidepressants or electroconvulsive therapy, but decreased in an animal model of depression and in brain tissue from depressed patients. Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates certain behaviors seen after antidepressant treatment in mice. p11 knockout mice exhibit a depression-like phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reactions to an antidepressant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Chergui, Karima -- Rachleff, Ilan -- Flajolet, Marc -- Zhang, Xiaoqun -- El Yacoubi, Malika -- Vaugeois, Jean-Marie -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):77-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400147" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; Annexin A2/genetics/*metabolism ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Cell Membrane/metabolism ; Depression/genetics/*metabolism ; Electroconvulsive Therapy ; Female ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Neurons/metabolism ; Rats ; Receptor, Serotonin, 5-HT1B/*metabolism ; S100 Proteins/genetics/*metabolism ; Serotonin/metabolism/physiology ; Signal Transduction ; Two-Hybrid System Techniques
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    A genome-wide association study identifies IL23R as an inflammatory bowel disease gene (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: The inflammatory bowel diseases Crohn's disease and ulcerative colitis are common, chronic disorders that cause abdominal pain, diarrhea, and gastrointestinal bleeding. To identify genetic factors that might contribute to these disorders, we performed a genome-wide association study. We found a highly significant association between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23. An uncommon coding variant (rs11209026, c.1142G〉A, p.Arg381Gln) confers strong protection against Crohn's disease, and additional noncoding IL23R variants are independently associated. Replication studies confirmed IL23R associations in independent cohorts of patients with Crohn's disease or ulcerative colitis. These results and previous studies on the proinflammatory role of IL-23 prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410764/" 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/PMC4410764/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duerr, Richard H -- Taylor, Kent D -- Brant, Steven R -- Rioux, John D -- Silverberg, Mark S -- Daly, Mark J -- Steinhart, A Hillary -- Abraham, Clara -- Regueiro, Miguel -- Griffiths, Anne -- Dassopoulos, Themistocles -- Bitton, Alain -- Yang, Huiying -- Targan, Stephan -- Datta, Lisa Wu -- Kistner, Emily O -- Schumm, L Philip -- Lee, Annette T -- Gregersen, Peter K -- Barmada, M Michael -- Rotter, Jerome I -- Nicolae, Dan L -- Cho, Judy H -- DK62413/DK/NIDDK NIH HHS/ -- DK62420/DK/NIDDK NIH HHS/ -- DK62422/DK/NIDDK NIH HHS/ -- DK62423/DK/NIDDK NIH HHS/ -- DK62429/DK/NIDDK NIH HHS/ -- DK62431/DK/NIDDK NIH HHS/ -- DK62432/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-019004/DK/NIDDK NIH HHS/ -- P30 DK063491-029004/DK/NIDDK NIH HHS/ -- P30 DK063491-039004/DK/NIDDK NIH HHS/ -- P30 DK063491-049004/DK/NIDDK NIH HHS/ -- U01 DK062420/DK/NIDDK NIH HHS/ -- U01 DK062422/DK/NIDDK NIH HHS/ -- U01 DK062423/DK/NIDDK NIH HHS/ -- U01 DK062429/DK/NIDDK NIH HHS/ -- U01 DK062432/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1461-3. Epub 2006 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center Presbyterian, Mezzanine Level, C-Wing, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068223" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Case-Control Studies ; Chromosomes, Human, Pair 1/genetics ; Cohort Studies ; Colitis, Ulcerative/genetics ; Crohn Disease/*genetics ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Testing ; Genome, Human ; Haplotypes ; Humans ; Interleukin-23/metabolism ; Jews/genetics ; Linkage Disequilibrium ; *Polymorphism, Single Nucleotide ; Receptors, Interleukin/*genetics/physiology ; Signal Transduction
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    Checkpoint proteins control survival of the postmitotic cells in Caenorhabditis elegans (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-03
    Description: Checkpoints are evolutionarily conserved signaling mechanisms that arrest cell division and alter cellular stress resistance in response to DNA damage or stalled replication forks. To study the consequences of loss of checkpoint functions in whole animals, checkpoint genes were inactivated in the nematode C. elegans. We show that checkpoint proteins are not only essential for normal development but also determine adult somatic maintenance. Checkpoint proteins play a role in the survival of postmitotic adult cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2568993/" 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/PMC2568993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olsen, Anders -- Vantipalli, Maithili C -- Lithgow, Gordon J -- AG21069/AG/NIA NIH HHS/ -- AG22868/AG/NIA NIH HHS/ -- NS050789-01/NS/NINDS NIH HHS/ -- R01 AG021069/AG/NIA NIH HHS/ -- R01 AG021069-04/AG/NIA NIH HHS/ -- R01 AG022868/AG/NIA NIH HHS/ -- R01 AG022868-04/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 2;312(5778):1381-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Buck Institute, 8001 Redwood Boulevard, Novato, CA 94945, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741121" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/genetics/physiology ; Animals ; Caenorhabditis elegans/cytology/growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/*physiology ; Cell Cycle Proteins/genetics/*physiology ; Cell Survival ; Heat-Shock Proteins/biosynthesis/genetics ; Mitosis/genetics/*physiology ; Mutation ; Protein Kinases/metabolism ; Schizosaccharomyces pombe Proteins ; Signal Transduction ; Stem Cells/cytology
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  • 14
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    Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate reward (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Norepinephrine (NE) is widely implicated in opiate withdrawal, but much less is known about its role in opiate-induced locomotion and reward. In mice lacking dopamine beta-hydroxylase (DBH), an enzyme critical for NE synthesis, we found that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomotion. These deficits were rescued by systemic NE restoration. Viral restoration of DBH expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for morphine. Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Valerie G -- Heusner, Carrie L -- Bland, Ross J -- During, Matthew J -- Weinshenker, David -- Palmiter, Richard D -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Conditioning (Psychology) ; Dopamine beta-Hydroxylase/genetics/metabolism ; Droxidopa/pharmacology ; Locomotion/drug effects ; Locus Coeruleus/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Morphine/*pharmacology ; Motor Activity/drug effects ; Norepinephrine/*physiology ; *Reward ; Signal Transduction ; Solitary Nucleus/*physiology ; *Synaptic Transmission
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    Cellular senescence in aging primates (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-02-04
    Description: The aging of organisms is characterized by a gradual functional decline of all organ systems. Mammalian somatic cells in culture display a limited proliferative life span, at the end of which they undergo an irreversible cell cycle arrest known as replicative senescence. Whether cellular senescence contributes to organismal aging has been controversial. We investigated telomere dysfunction, a recently discovered biomarker of cellular senescence, and found that the number of senescent fibroblasts increases exponentially in the skin of aging baboons, reaching 〉15% of all cells in very old individuals. In addition, the same cells contain activated ataxia-telangiectasia mutated kinase and heterochromatinized nuclei, confirming their senescent status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herbig, Utz -- Ferreira, Mark -- Condel, Laura -- Carey, Dee -- Sedivy, John M -- F32 CA099388/CA/NCI NIH HHS/ -- P01 HL028972/HL/NHLBI NIH HHS/ -- P20 RR015578/RR/NCRR NIH HHS/ -- P51 RR013986/RR/NCRR NIH HHS/ -- R01 AG016694/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1257. Epub 2006 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02903, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456035" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Biomarkers ; Cell Aging/*physiology ; Cell Cycle Proteins/metabolism ; DNA Damage ; DNA Replication ; DNA-Binding Proteins/metabolism ; Dermis/cytology ; Female ; Fibroblasts/cytology/*physiology ; Heterochromatin/metabolism ; Male ; Oxidative Stress ; Papio/*physiology ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Telomere/physiology ; Tumor Suppressor Proteins/metabolism
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    Developmental biology. The Turing model comes of molecular age (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383235/" 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/PMC4383235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maini, Philip K -- Baker, Ruth E -- Chuong, Cheng-Ming -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR042177-11/AR/NIAMS NIH HHS/ -- R01 AR042177-12/AR/NIAMS NIH HHS/ -- R01 AR047364/AR/NIAMS NIH HHS/ -- R01 AR047364-04/AR/NIAMS NIH HHS/ -- R01 AR047364-05/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1397-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Mathematical Biology, University of Oxford, Oxford OX1 3LB, UK. maini@maths.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17138885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Diffusion ; Hair Follicle/*growth & development/metabolism ; Intercellular Signaling Peptides and Proteins/*metabolism ; Mathematics ; Mice ; *Models, Biological ; Signal Transduction ; Wnt Proteins/*metabolism
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  • 17
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    Escherichia coli induces DNA double-strand breaks in eukaryotic cells (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-12
    Description: Transient infection of eukaryotic cells with commensal and extraintestinal pathogenic Escherichia coli of phylogenetic group B2 blocks mitosis and induces megalocytosis. This trait is linked to a widely spread genomic island that encodes giant modular nonribosomal peptide and polyketide synthases. Contact with E. coli expressing this gene cluster causes DNA double-strand breaks and activation of the DNA damage checkpoint pathway, leading to cell cycle arrest and eventually to cell death. Discovery of hybrid peptide-polyketide genotoxins in E. coli will change our view on pathogenesis and commensalism and open new biotechnological applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nougayrede, Jean-Philippe -- Homburg, Stefan -- Taieb, Frederic -- Boury, Michele -- Brzuszkiewicz, Elzbieta -- Gottschalk, Gerhard -- Buchrieser, Carmen -- Hacker, Jorg -- Dobrindt, Ulrich -- Oswald, Eric -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INRA, UMR1225, Ecole Nationale Veterinaire de Toulouse, Toulouse F-31076, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/chemistry ; Cytotoxins/*metabolism ; DNA/analysis ; *DNA Damage ; DNA-Binding Proteins/metabolism ; Escherichia coli/genetics/*pathogenicity/*physiology ; G2 Phase ; *Genomic Islands ; HeLa Cells ; Histones/metabolism ; Humans ; Intestinal Mucosa/cytology/microbiology ; Molecular Sequence Data ; Mutagenesis ; Mutagens/*metabolism ; Peptides/*metabolism ; Phosphorylation ; Polyketide Synthases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
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  • 18
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    Volatile signaling in plant-plant interactions: "talking trees" in the genomics era (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-14
    Description: Plants may "eavesdrop" on volatile organic compounds (VOCs) released by herbivore-attacked neighbors to activate defenses before being attacked themselves. Transcriptome and signal cascade analyses of VOC-exposed plants suggest that plants eavesdrop to prime direct and indirect defenses and to hone competitive abilities. Advances in research on VOC biosynthesis and perception have facilitated the production of plants that are genetically "deaf" to particular VOCs or "mute" in elements of their volatile vocabulary. Such plants, together with advances in VOC analytical instrumentation, will allow researchers to determine whether fluency enhances the fitness of plants in natural communities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldwin, Ian T -- Halitschke, Rayko -- Paschold, Anja -- von Dahl, Caroline C -- Preston, Catherine A -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):812-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans Knoll Strasse 8, Jena 07745, Germany. baldwin@ice.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469918" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Diffusion ; Gene Expression Regulation, Plant ; Genomics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Organic Chemicals/*metabolism ; Plant Leaves/metabolism ; *Plant Physiological Phenomena ; Plants/*genetics/metabolism ; Signal Transduction ; Volatilization
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  • 19
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    Caveolin-1 is essential for liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-09-16
    Description: Liver regeneration is an orchestrated cellular response that coordinates cell activation, lipid metabolism, and cell division. We found that caveolin-1 gene-disrupted mice (cav1-/- mice) exhibited impaired liver regeneration and low survival after a partial hepatectomy. Hepatocytes showed dramatically reduced lipid droplet accumulation and did not advance through the cell division cycle. Treatment of cav1-/- mice with glucose (which is a predominant energy substrate when compared to lipids) drastically increased survival and reestablished progression of the cell cycle. Thus, caveolin-1 plays a crucial role in the mechanisms that coordinate lipid metabolism with the proliferative response occurring in the liver after cellular injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Manuel A -- Albor, Cecilia -- Ingelmo-Torres, Mercedes -- Nixon, Susan J -- Ferguson, Charles -- Kurzchalia, Teymuras -- Tebar, Francesc -- Enrich, Carlos -- Parton, Robert G -- Pol, Albert -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Cellular, Facultat de Medicina, Institut d'Investigacions Biomediques August Pi i Sunyer, Universitat de Barcelona, Casanova 143, 08036 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Division ; Fatty Acids/blood/metabolism ; Glucose/administration & dosage ; Hepatectomy ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/cytology/*metabolism ; *Lipid Metabolism ; Lipids/blood ; Liver/metabolism/ultrastructure ; *Liver Regeneration ; Male ; Mice ; Phosphorylation ; RNA, Small Interfering ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Triglycerides/blood/metabolism
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  • 20
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    CDK2-dependent phosphorylation of FOXO1 as an apoptotic response to DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: The function of cyclin-dependent kinase 2 (CDK2) is often abolished after DNA damage. The inhibition of CDK2 plays a central role in DNA damage-induced cell cycle arrest and DNA repair. However, whether CDK2 also influences the survival of cells under genotoxic stress is unknown. Forkhead box O (FOXO) transcription factors are emerging as key regulators of cell survival. CDK2 specifically phosphorylated FOXO1 at serine-249 (Ser249) in vitro and in vivo. Phosphorylation of Ser249 resulted in cytoplasmic localization and inhibition of FOXO1. This phosphorylation was abrogated upon DNA damage through the cell cycle checkpoint pathway that is dependent on the protein kinases Chk1 and Chk2. Moreover, silencing of FOXO1 by small interfering RNA diminished DNA damage-induced death in both p53-deficient and p53-proficient cells. This effect was reversed by restored expression of FOXO1 in a manner depending on phosphorylation of Ser249. Functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Haojie -- Regan, Kevin M -- Lou, Zhenkun -- Chen, Junjie -- Tindall, Donald J -- CA91956/CA/NCI NIH HHS/ -- DK60920/DK/NIDDK NIH HHS/ -- DK65236/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Camptothecin/pharmacology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/genetics/*metabolism ; Cytoplasm/metabolism ; *DNA Damage ; Forkhead Transcription Factors/antagonists & inhibitors/*metabolism ; Humans ; Mice ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/metabolism
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    Neuroscience. Brain evolution on the far side (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):244-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Brain/physiology ; Brain Chemistry ; Cognition ; Evolution, Molecular ; Gene Expression Profiling ; Humans ; Invertebrates/anatomy & histology/physiology ; Membrane Proteins/*analysis/genetics/metabolism ; Multiprotein Complexes/*analysis/genetics/metabolism ; Nerve Tissue Proteins/*analysis/genetics/metabolism ; Organ Size ; Receptors, Neurotransmitter/analysis/genetics/metabolism ; Signal Transduction ; Synaptic Membranes/*chemistry/physiology ; Synaptic Transmission ; Vertebrates/anatomy & histology/physiology
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    B cell ligand discrimination through a spreading and contraction response (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-05-06
    Description: B cells recognize foreign antigens by virtue of cell surface immunoglobulin receptors and are most effectively activated by membrane-bound ligands. Here, we show that in the early stages of this process, B cells exhibit a two-phase response in which they first spread over the antigen-bearing membrane and then contract, thereby collecting bound antigen into a central aggregate. The extent of this response, which is both signaling- and actin-dependent, determines the quantity of antigen accumulated and hence the degree of B cell activation. Brownian dynamic simulations reproduce essential features of the antigen collection process and suggest a possible basis for affinity discrimination. We propose that dynamic spreading is an important step of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fleire, S J -- Goldman, J P -- Carrasco, Y R -- Weber, M -- Bray, D -- Batista, F D -- G64713/PHS HHS/ -- New York, N.Y. -- Science. 2006 May 5;312(5774):738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675699" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Algorithms ; Animals ; Antibody Affinity ; Antigen Presentation ; Antigens, Surface/*immunology ; B-Lymphocytes/*immunology/*physiology ; Cell Shape ; Computer Simulation ; Flow Cytometry ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence ; Models, Immunological ; Muramidase/immunology ; Receptors, Antigen, B-Cell/*immunology/metabolism ; Recombinant Fusion Proteins/immunology ; Signal Transduction ; Stochastic Processes ; T-Lymphocytes/immunology
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    A plant peptide encoded by CLV3 identified by in situ MALDI-TOF MS analysis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: The Arabidopsis CLAVATA3 (CLV3) gene encodes a stem cell-specific protein presumed to be a precursor of a secreted peptide hormone. Matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS) applied to in situ Arabidopsis tissues determined the structure of a modified 12-amino acid peptide (MCLV3), which was derived from a conserved motif in the CLV3 sequence. Synthetic MCLV3 induced shoot and root meristem consumption as cells differentiated into other organs, displaying the typical phenotype of transgenic plants overexpressing CLV3. These results suggest that the functional peptide of CLV3 is MCLV3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, Tatsuhiko -- Sawa, Shinichiro -- Kinoshita, Atsuko -- Mizuno, Satoko -- Kakimoto, Tatsuo -- Fukuda, Hiroo -- Sakagami, Youji -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya, 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902141" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/*cytology/genetics/metabolism ; Arabidopsis Proteins/*chemistry/genetics/*metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Hydroxyproline/chemistry ; Meristem/*cytology/drug effects/metabolism ; Molecular Sequence Data ; Oligopeptides/chemistry/*metabolism/pharmacology ; Plant Roots/growth & development ; Plants, Genetically Modified ; Signal Transduction ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Stem Cells/cytology
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    Synaptic amplifier of inflammatory pain in the spinal dorsal horn (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Stark, Johanna -- Fischer, Harald -- Wagner, Matthias -- Drdla, Ruth -- Jager, Tino -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Inflammation/*physiopathology ; Long-Term Potentiation ; Nerve Fibers, Unmyelinated/*physiology ; Neuronal Plasticity ; Nitric Oxide/physiology ; Pain/*physiopathology ; Patch-Clamp Techniques ; Periaqueductal Gray/physiology ; Posterior Horn Cells/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Spinal Cord/physiopathology ; Synapses/physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulatory blueprint for a chordate embryo (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: Ciona is an emerging model system for elucidating gene networks in development. Comprehensive in situ hybridization assays have identified 76 regulatory genes with localized expression patterns in the early embryo, at the time when naive blastomeres are determined to follow specific cell fates. Systematic gene disruption assays provided more than 3000 combinations of gene expression profiles in mutant backgrounds. Deduced gene circuit diagrams describing the formation of larval tissues were computationally visualized. These diagrams constitute a blueprint for the Ciona embryo and provide a foundation for understanding the evolutionary origins of the chordate body plan.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Kaoru S -- Levine, Michael -- Satoh, Nori -- Satou, Yutaka -- New York, N.Y. -- Science. 2006 May 26;312(5777):1183-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, 606-8502, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Blastomeres/cytology/physiology ; Body Patterning/genetics ; Cell Differentiation/genetics ; Cell Lineage ; Ciona intestinalis/*embryology/*genetics ; Computational Biology ; Embryo, Nonmammalian/*physiology ; Embryonic Development/*genetics ; Epidermis/cytology ; Gastrula/cytology/physiology ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Regulator ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins/*genetics/physiology ; Neurons/cytology ; Nodal Protein ; Notochord/embryology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Transcription Factors/*genetics/physiology ; Transcription, Genetic ; Transforming Growth Factor beta/genetics/physiology
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    Mutations that increase the life span of C. elegans inhibit tumor growth (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-19
    Description: Mutations in gld-1 cause lethal germline tumors in the nematode Caenorhabditis elegans. We find that a wide variety of mutations that extend C. elegans' life span confer resistance to these tumors. The long life spans of daf-2/insulin-receptor mutants were not shortened at all by gld-1 mutations; we attribute this finding to decreased cell division and increased DAF-16/p53-dependent apoptosis within the tumors. Mutations that increase life span by restricting food intake or inhibiting respiration did not affect apoptosis but reduced tumor cell division. Unexpectedly, none of these longevity mutations affected mitosis in normal germlines; this finding suggests that cellular changes that lead to longevity preferentially antagonize tumor cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinkston, Julie M -- Garigan, Delia -- Hansen, Malene -- Kenyon, Cynthia -- AG000278/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):971-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, 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/16917064" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Caenorhabditis elegans/*genetics/physiology ; Caenorhabditis elegans Proteins/*genetics/physiology ; Caloric Restriction ; Cell Proliferation ; Forkhead Transcription Factors ; Genes, Helminth ; Germ Cells/cytology ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity/*genetics ; Mitochondria/metabolism ; Models, Animal ; *Mutation ; Neoplasms/genetics/*pathology ; Oogenesis ; Receptor, Insulin/*genetics/physiology ; Reproduction ; Signal Transduction ; Transcription Factors/genetics/physiology
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    RNA interference directs innate immunity against viruses in adult Drosophila (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: Innate immunity against bacterial and fungal pathogens is mediated by Toll and immune deficiency (Imd) pathways, but little is known about the antiviral response in Drosophila. Here, we demonstrate that an RNA interference pathway protects adult flies from infection by two evolutionarily diverse viruses. Our work also describes a molecular framework for the viral immunity, in which viral double-stranded RNA produced during infection acts as the pathogen trigger whereas Drosophila Dicer-2 and Argonaute-2 act as host sensor and effector, respectively. These findings establish a Drosophila model for studying the innate immunity against viruses in animals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1509097/" 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/PMC1509097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiao-Hong -- Aliyari, Roghiyh -- Li, Wan-Xiang -- Li, Hong-Wei -- Kim, Kevin -- Carthew, Richard -- Atkinson, Peter -- Ding, Shou-Wei -- AI052447/AI/NIAID NIH HHS/ -- R01 AI052447/AI/NIAID NIH HHS/ -- R01 GM068743/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):452-4. Epub 2006 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program for Microbiology, University of California, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Cell Line ; Drosophila Proteins/genetics/metabolism/physiology ; Drosophila melanogaster/embryology/genetics/*immunology/*virology ; Embryo, Nonmammalian/immunology/virology ; Escherichia coli/physiology ; *Immunity, Innate ; Insect Viruses/genetics/*physiology ; Micrococcus luteus/physiology ; Mutation ; Nodaviridae/*physiology ; RNA Helicases/genetics/metabolism ; *RNA Interference ; RNA Viruses/genetics/physiology ; RNA, Double-Stranded/metabolism ; RNA, Small Interfering/metabolism ; RNA, Viral/genetics/metabolism ; RNA-Binding Proteins/genetics/physiology ; RNA-Induced Silencing Complex/genetics/physiology ; Ribonuclease III ; Signal Transduction ; Toll-Like Receptors/physiology ; Transfection ; Virus Replication
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    Plant science. Auxin begins to give up its secrets (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1230-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946049" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*growth & development/metabolism ; Arabidopsis Proteins/chemistry/*metabolism ; Bacteria/metabolism ; Bacterial Physiological Phenomena ; Computer Simulation ; F-Box Proteins/chemistry/*metabolism ; Gene Expression Regulation, Plant ; Indoleacetic Acids/*metabolism ; MicroRNAs/metabolism ; Models, Biological ; *Plant Development ; Plant Growth Regulators/*metabolism ; Plant Proteins/*metabolism ; Plants/genetics/metabolism/microbiology ; RNA Interference ; RNA, Plant/metabolism ; Receptors, Cell Surface/chemistry/*metabolism ; Signal Transduction
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    Developmental biology. How many ways to make a chordate? (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lemaire, Patrick -- New York, N.Y. -- Science. 2006 May 26;312(5777):1145-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie du Developpement de Marseille Luminy, UMR6216 CNRS-Universite de la Mediterranee, Campus de Luminy, F-13288 Marseille cedex 9, France. lemaire@ibdm.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Body Patterning/genetics ; Cell Differentiation/genetics ; Ciona intestinalis/*embryology/*genetics ; Embryo, Nonmammalian/physiology ; Embryonic Development/*genetics ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Regulator ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins/*genetics/physiology ; Ligands ; Polymerase Chain Reaction ; Signal Transduction ; Transcription Factors/*genetics/physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Role of leucine in regulating food intake (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laviano, Alessandro -- Meguid, Michael M -- Inui, Akio -- Rossi-Fanelli, Filippo -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1236-8; author reply 1236-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Appetite ; Brain/metabolism ; *Eating ; Humans ; Leucine/*administration & dosage/*physiology ; *Protein Biosynthesis ; Protein Kinases/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases
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    Virology. Sensing viral RNA amid your own (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujita, Takashi -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):935-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto 606- 8507, Japan. tfujita@virus.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095686" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/chemistry/*metabolism ; Humans ; Immunity, Innate ; Interferons/biosynthesis ; Nucleic Acid Conformation ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/chemistry/metabolism ; RNA, Viral/chemistry/*metabolism ; Signal Transduction ; Toll-Like Receptors/metabolism ; Viral Nonstructural Proteins/metabolism ; Virus Diseases/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Yersinia YopJ acetylates and inhibits kinase activation by blocking phosphorylation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: Yersinia species use a variety of type III effector proteins to target eukaryotic signaling systems. The effector YopJ inhibits mitogen-activated protein kinase (MAPK) and the nuclear factor kappaB (NFkappaB) signaling pathways used in innate immune response by preventing activation of the family of MAPK kinases (MAPKK). We show that YopJ acted as an acetyltransferase, using acetyl-coenzyme A (CoA) to modify the critical serine and threonine residues in the activation loop of MAPKK6 and thereby blocking phosphorylation. The acetylation on MAPKK6 directly competed with phosphorylation, preventing activation of the modified protein. This covalent modification may be used as a general regulatory mechanism in biological signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukherjee, Sohini -- Keitany, Gladys -- Li, Yan -- Wang, Yong -- Ball, Haydn L -- Goldsmith, Elizabeth J -- Orth, Kim -- R01-AI056404/AI/NIAID NIH HHS/ -- R21-DK072134/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1211-4.〈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/16728640" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl Coenzyme A/metabolism ; Acetylation ; Acetyltransferases/metabolism ; Bacterial Proteins/*metabolism ; Catalytic Domain ; Cell Line ; Cell-Free System ; Electrophoresis, Polyacrylamide Gel ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase 6/chemistry/*metabolism ; MAP Kinase Signaling System ; NF-kappa B/metabolism ; Phosphorylation ; Recombinant Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Yersinia/*metabolism/pathogenicity
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    Type 1 interferons and the virus-host relationship: a lesson in detente (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-13
    Description: The interface between an infectious agent and its host represents the ultimate battleground for survival: The microbe must secure a niche for replication, whereas the host must limit the pathogen's advance. Among the host's arsenal of antimicrobial factors, the type 1 interferons (IFNs) induce potent defense mechanisms against viruses and are key in the host-virus standoff. Viruses have evolved multiple tricks to avoid the immediate antiviral effects of IFNs and, in turn, hosts have adapted use of this innate cytokine system to galvanize multiple additional layers of immune defense. The plasticity that exists in these interactions provides us with a lesson in detente.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Sastre, Adolfo -- Biron, Christine A -- P01AI52106/AI/NIAID NIH HHS/ -- P01AI58113/AI/NIAID NIH HHS/ -- R01AI46954/AI/NIAID NIH HHS/ -- R01AI55677/AI/NIAID NIH HHS/ -- R01CA41268/CA/NCI NIH HHS/ -- U19AI62623/AI/NIAID NIH HHS/ -- U54AI57158/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 May 12;312(5775):879-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/physiology ; *Immunity, Innate ; Interferon Regulatory Factors/physiology ; Interferon Type I/biosynthesis/genetics/*physiology ; Models, Biological ; RNA Helicases/metabolism ; Signal Transduction ; Toll-Like Receptors/physiology ; Viral Proteins/metabolism ; *Virus Physiological Phenomena ; Viruses/*immunology
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    The genome of the sea urchin Strongylocentrotus purpuratus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-11
    Description: We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus, a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159423/" 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/PMC3159423/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sea Urchin Genome Sequencing Consortium -- Sodergren, Erica -- Weinstock, George M -- Davidson, Eric H -- Cameron, R Andrew -- Gibbs, Richard A -- Angerer, Robert C -- Angerer, Lynne M -- Arnone, Maria Ina -- Burgess, David R -- Burke, Robert D -- Coffman, James A -- Dean, Michael -- Elphick, Maurice R -- Ettensohn, Charles A -- Foltz, Kathy R -- Hamdoun, Amro -- Hynes, Richard O -- Klein, William H -- Marzluff, William -- McClay, David R -- Morris, Robert L -- Mushegian, Arcady -- Rast, Jonathan P -- Smith, L Courtney -- Thorndyke, Michael C -- Vacquier, Victor D -- Wessel, Gary M -- Wray, Greg -- Zhang, Lan -- Elsik, Christine G -- Ermolaeva, Olga -- Hlavina, Wratko -- Hofmann, Gretchen -- Kitts, Paul -- Landrum, Melissa J -- Mackey, Aaron J -- Maglott, Donna -- Panopoulou, Georgia -- Poustka, Albert J -- Pruitt, Kim -- Sapojnikov, Victor -- Song, Xingzhi -- Souvorov, Alexandre -- Solovyev, Victor -- Wei, Zheng -- Whittaker, Charles A -- Worley, Kim -- Durbin, K James -- Shen, Yufeng -- Fedrigo, Olivier -- Garfield, David -- Haygood, Ralph -- Primus, Alexander -- Satija, Rahul -- Severson, Tonya -- Gonzalez-Garay, Manuel L -- Jackson, Andrew R -- Milosavljevic, Aleksandar -- Tong, Mark -- Killian, Christopher E -- Livingston, Brian T -- Wilt, Fred H -- Adams, Nikki -- Belle, Robert -- Carbonneau, Seth -- Cheung, Rocky -- Cormier, Patrick -- Cosson, Bertrand -- Croce, Jenifer -- Fernandez-Guerra, Antonio -- Geneviere, Anne-Marie -- Goel, Manisha -- Kelkar, Hemant -- Morales, Julia -- Mulner-Lorillon, Odile -- Robertson, Anthony J -- Goldstone, Jared V -- Cole, Bryan -- Epel, David -- Gold, Bert -- Hahn, Mark E -- Howard-Ashby, Meredith -- Scally, Mark -- Stegeman, John J -- Allgood, Erin L -- Cool, Jonah -- Judkins, Kyle M -- McCafferty, Shawn S -- Musante, Ashlan M -- Obar, Robert A -- Rawson, Amanda P -- Rossetti, Blair J -- Gibbons, Ian R -- Hoffman, Matthew P -- Leone, Andrew -- Istrail, Sorin -- Materna, Stefan C -- Samanta, Manoj P -- Stolc, Viktor -- Tongprasit, Waraporn -- Tu, Qiang -- Bergeron, Karl-Frederik -- Brandhorst, Bruce P -- Whittle, James -- Berney, Kevin -- Bottjer, David J -- Calestani, Cristina -- Peterson, Kevin -- Chow, Elly -- Yuan, Qiu Autumn -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Bosdet, Ian -- Heesun, Shin -- Marra, Marco A -- Schein, Jacqueline -- Anderson, Michele K -- Brockton, Virginia -- Buckley, Katherine M -- Cohen, Avis H -- Fugmann, Sebastian D -- Hibino, Taku -- Loza-Coll, Mariano -- Majeske, Audrey J -- Messier, Cynthia -- Nair, Sham V -- Pancer, Zeev -- Terwilliger, David P -- Agca, Cavit -- Arboleda, Enrique -- Chen, Nansheng -- Churcher, Allison M -- Hallbook, F -- Humphrey, Glen W -- Idris, Mohammed M -- Kiyama, Takae -- Liang, Shuguang -- Mellott, Dan -- Mu, Xiuqian -- Murray, Greg -- Olinski, Robert P -- Raible, Florian -- Rowe, Matthew -- Taylor, John S -- Tessmar-Raible, Kristin -- Wang, D -- Wilson, Karen H -- Yaguchi, Shunsuke -- Gaasterland, Terry -- Galindo, Blanca E -- Gunaratne, Herath J -- Juliano, Celina -- Kinukawa, Masashi -- Moy, Gary W -- Neill, Anna T -- Nomura, Mamoru -- Raisch, Michael -- Reade, Anna -- Roux, Michelle M -- Song, Jia L -- Su, Yi-Hsien -- Townley, Ian K -- Voronina, Ekaterina -- Wong, Julian L -- Amore, Gabriele -- Branno, Margherita -- Brown, Euan R -- Cavalieri, Vincenzo -- Duboc, Veronique -- Duloquin, Louise -- Flytzanis, Constantin -- Gache, Christian -- Lapraz, Francois -- Lepage, Thierry -- Locascio, Annamaria -- Martinez, Pedro -- Matassi, Giorgio -- Matranga, Valeria -- Range, Ryan -- Rizzo, Francesca -- Rottinger, Eric -- Beane, Wendy -- Bradham, Cynthia -- Byrum, Christine -- Glenn, Tom -- Hussain, Sofia -- Manning, Gerard -- Miranda, Esther -- Thomason, Rebecca -- Walton, Katherine -- Wikramanayke, Athula -- Wu, Shu-Yu -- Xu, Ronghui -- Brown, C Titus -- Chen, Lili -- Gray, Rachel F -- Lee, Pei Yun -- Nam, Jongmin -- Oliveri, Paola -- Smith, Joel -- Muzny, Donna -- Bell, Stephanie -- Chacko, Joseph -- Cree, Andrew -- Curry, Stacey -- Davis, Clay -- Dinh, Huyen -- Dugan-Rocha, Shannon -- Fowler, Jerry -- Gill, Rachel -- Hamilton, Cerrissa -- Hernandez, Judith -- Hines, Sandra -- Hume, Jennifer -- Jackson, Laronda -- Jolivet, Angela -- Kovar, Christie -- Lee, Sandra -- Lewis, Lora -- Miner, George -- Morgan, Margaret -- Nazareth, Lynne V -- Okwuonu, Geoffrey -- Parker, David -- Pu, Ling-Ling -- Thorn, Rachel -- Wright, Rita -- 2P42 ESO7381/PHS HHS/ -- 5 U54 HG003273/HG/NHGRI NIH HHS/ -- EY11930/EY/NEI NIH HHS/ -- F32 ESO12794/PHS HHS/ -- F32 HD047136/HD/NICHD NIH HHS/ -- F32 HD047136-02/HD/NICHD NIH HHS/ -- F32 HD047136-03/HD/NICHD NIH HHS/ -- F32-HD47136/HD/NICHD NIH HHS/ -- GM058231/GM/NIGMS NIH HHS/ -- GM070840/GM/NIGMS NIH HHS/ -- GM61005/GM/NIGMS NIH HHS/ -- GM61464/GM/NIGMS NIH HHS/ -- HD-37105/HD/NICHD NIH HHS/ -- HD039948/HD/NICHD NIH HHS/ -- HD14483/HD/NICHD NIH HHS/ -- HD66219/HD/NICHD NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 ES006272/ES/NIEHS NIH HHS/ -- R01 ES006272-13/ES/NIEHS NIH HHS/ -- R01 GM070840/GM/NIGMS NIH HHS/ -- R01 HD028152/HD/NICHD NIH HHS/ -- R01ES006272/ES/NIEHS NIH HHS/ -- R37-HD12896/HD/NICHD NIH HHS/ -- RR-15044/RR/NCRR NIH HHS/ -- S19916/Biotechnology and Biological Sciences Research Council/United Kingdom -- T32 GM007601/GM/NIGMS NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):941-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095691" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcification, Physiologic ; Cell Adhesion Molecules/genetics/physiology ; Complement Activation/genetics ; Computational Biology ; Embryonic Development/genetics ; Evolution, Molecular ; Gene Expression Regulation, Developmental ; Genes ; *Genome ; Immunity, Innate/genetics ; Immunologic Factors/genetics/physiology ; Male ; Nervous System Physiological Phenomena ; Proteins/genetics/physiology ; *Sequence Analysis, DNA ; Signal Transduction ; Strongylocentrotus purpuratus/embryology/*genetics/immunology/physiology ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immunology. Targeting the tolls (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, Ingrid -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):184-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614188" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Animals ; Autoimmune Diseases/drug therapy/*immunology ; Coronary Artery Disease/drug therapy/immunology ; Humans ; Hypersensitivity/drug therapy/*immunology ; *Immunity, Innate ; Infection/drug therapy/*immunology ; Inflammation/drug therapy/*immunology ; Mice ; Mutation ; Sepsis/drug therapy/immunology ; Signal Transduction ; Toll-Like Receptors/antagonists & inhibitors/genetics/*immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Waking experience affects sleep need in Drosophila (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Sleep is a vital, evolutionarily conserved phenomenon, whose function is unclear. Although mounting evidence supports a role for sleep in the consolidation of memories, until now, a molecular connection between sleep, plasticity, and memory formation has been difficult to demonstrate. We establish Drosophila as a model to investigate this relation and demonstrate that the intensity and/or complexity of prior social experience stably modifies sleep need and architecture. Furthermore, this experience-dependent plasticity in sleep need is subserved by the dopaminergic and adenosine 3',5'-monophosphate signaling pathways and a particular subset of 17 long-term memory genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ganguly-Fitzgerald, Indrani -- Donlea, Jeff -- Shaw, Paul J -- R01-NS051305-01A1/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1775-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurosciences Institute, 10640 John Jay Hopkins Drive, San Diego, CA 92101, USA. transposase@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Chemistry ; Circadian Rhythm ; Cyclic AMP/metabolism ; Dopamine/analysis/metabolism ; Drosophila melanogaster/genetics/growth & development/*physiology ; Female ; Hearing ; Learning ; Male ; Memory ; *Models, Animal ; Mutation ; Sexual Behavior, Animal ; Signal Transduction ; *Sleep ; Smell ; Social Environment ; Social Isolation ; Vision, Ocular
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hox control of organ size by regulation of morphogen production and mobility (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-03
    Description: Selector genes modify developmental pathways to sculpt animal body parts. Although body parts differ in size, the ways in which selector genes create size differences are unknown. We have studied how the Drosophila Hox gene Ultrabithorax (Ubx) limits the size of the haltere, which, by the end of larval development, has approximately fivefold fewer cells than the wing. We find that Ubx controls haltere size by restricting both the transcription and the mobility of the morphogen Decapentaplegic (Dpp). Ubx restricts Dpp's distribution in the haltere by increasing the amounts of the Dpp receptor, thickveins. Because morphogens control tissue growth in many contexts, these findings provide a potentially general mechanism for how selector genes modify organ sizes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628481/" 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/PMC2628481/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crickmore, Michael A -- Mann, Richard S -- R01 GM054510/GM/NIGMS NIH HHS/ -- R01 GM054510-12/GM/NIGMS NIH HHS/ -- R01 GM054510-13/GM/NIGMS NIH HHS/ -- R01 GM054510-14/GM/NIGMS NIH HHS/ -- R01 GM058575/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):63-8. Epub 2006 Jun 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Drosophila Proteins/*genetics/*metabolism/*physiology ; Drosophila melanogaster/anatomy & histology/*genetics/*growth & ; development/metabolism ; Gene Expression Regulation, Developmental ; Genes, Insect ; Homeodomain Proteins/*genetics/*physiology ; Morphogenesis ; Organ Size ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Receptors, Cell Surface/genetics/metabolism ; Signal Transduction ; Transcription Factors/*genetics/*physiology ; Transcription, Genetic ; Up-Regulation ; Wings, Animal/cytology/*growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Developmental biology. Morphing into shape (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-11
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2973999/" 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/PMC2973999/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, David L -- R01 GM063622/GM/NIGMS NIH HHS/ -- R01 GM063622-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):50-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. dstern@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Body Size ; Cell Proliferation ; Drosophila Proteins/*genetics/*metabolism/physiology ; Drosophila melanogaster/anatomy & histology/*genetics/*growth & ; development/metabolism ; Gene Expression Regulation, Developmental ; Genes, Insect ; Homeodomain Proteins/*genetics/physiology ; Morphogenesis ; Organ Size ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Transcription Factors/*genetics/physiology ; Wings, Animal/cytology/*growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Stem cells and their niches (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: A constellation of intrinsic and extrinsic cellular mechanisms regulates the balance of self-renewal and differentiation in all stem cells. Stem cells, their progeny, and elements of their microenvironment make up an anatomical structure that coordinates normal homeostatic production of functional mature cells. Here we discuss the stem cell niche concept, highlight recent progress, and identify important unanswered questions. We focus on three mammalian stem cell systems where large numbers of mature cells must be continuously produced throughout adult life: intestinal epithelium, epidermal structures, and bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Kateri A -- Lemischka, Ihor R -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1880-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, NJ 08544, USA. kamoore@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/cytology/physiology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Dermis/cytology/physiology ; Epidermis/cytology/physiology ; Hair Follicle/*cytology ; Hematopoietic Stem Cells/*cytology/*physiology ; Homeostasis ; Intestinal Mucosa/*cytology ; Mesoderm/cytology/physiology ; Multipotent Stem Cells/cytology/physiology ; Osteoblasts/physiology ; Signal Transduction ; Stem Cell Transplantation ; 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
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    Immunology. Discriminating microbe from self suffers a double toll (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodnow, Christopher C -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1606-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉John Curtin School of Medical Research and Australian Phenomics Facility, Australian National University, Post Office Box 334, Canberra, ACT 0200, Australia. chris.goodnow@anu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Ly/genetics/physiology ; Autoantibodies/biosynthesis ; *Autoimmunity ; B-Lymphocytes/immunology ; Dendritic Cells/immunology ; Gene Dosage ; Gene Duplication ; Humans ; Interferon-alpha/biosynthesis ; Lupus Erythematosus, Systemic/genetics/*immunology ; Lymphocyte Activation ; Membrane Glycoproteins/genetics/*immunology ; Mice ; Multifactorial Inheritance ; RNA Splicing ; Receptors, Antigen, B-Cell/immunology ; Receptors, IgG/genetics/immunology ; Self Tolerance ; Signal Transduction ; Toll-Like Receptor 7/genetics/*immunology ; Toll-Like Receptor 9/*immunology ; Y Chromosome/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Microbiology. Bacteria seize control by acetylating host proteins (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Worby, Carolyn A -- Dixon, Jack E -- New York, N.Y. -- Science. 2006 May 26;312(5777):1150-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16731519" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/metabolism ; Bacterial Proteins/*metabolism ; Enzyme Activation ; Humans ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 6/*metabolism ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Models, Biological ; NF-kappa B/metabolism ; Phosphorylation ; SUMO-1 Protein/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Yersinia/*metabolism/pathogenicity ; Yersinia pestis/metabolism/pathogenicity ; p38 Mitogen-Activated Protein Kinases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A systems approach to mapping DNA damage response pathways (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-20
    Description: Failure of cells to respond to DNA damage is a primary event associated with mutagenesis and environmental toxicity. To map the transcriptional network controlling the damage response, we measured genomewide binding locations for 30 damage-related transcription factors (TFs) after exposure of yeast to methyl-methanesulfonate (MMS). The resulting 5272 TF-target interactions revealed extensive changes in the pattern of promoter binding and identified damage-specific binding motifs. As systematic functional validation, we identified interactions for which the target changed expression in wild-type cells in response to MMS but was nonresponsive in cells lacking the TF. Validated interactions were assembled into causal pathway models that provide global hypotheses of how signaling, transcription, and phenotype are integrated after damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811083/" 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/PMC2811083/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Workman, Christopher T -- Mak, H Craig -- McCuine, Scott -- Tagne, Jean-Bosco -- Agarwal, Maya -- Ozier, Owen -- Begley, Thomas J -- Samson, Leona D -- Ideker, Trey -- R01 ES014811/ES/NIEHS NIH HHS/ -- R01 ES014811-01A1/ES/NIEHS NIH HHS/ -- R01 GM070743/GM/NIGMS NIH HHS/ -- R01 GM070743-01/GM/NIGMS NIH HHS/ -- R01 GM070743-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 19;312(5776):1054-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709784" target="_blank"〉PubMed〈/a〉
    Keywords: *DNA Damage ; DNA Repair/genetics/physiology ; DNA, Fungal ; Fungal Proteins/metabolism ; Gene Expression Regulation, Fungal ; Methyl Methanesulfonate ; Promoter Regions, Genetic ; Protein Binding ; Saccharomyces ; Signal Transduction ; Systems Theory ; Transcription Factors/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 43
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    Comment on "PDK1 nucleates T cell receptor-induced signaling complex for NF-kappaB activation" (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: We observe that protein kinase C (PKC) is phosphorylated on the activation loop at threonine 538 (Thr-538) before T cell activation. Our results are inconsistent with the conclusions of Lee et al. (Reports, 1 April 2005, p. 114) that the Thr-538 phosphorylation of PKC is regulated by T cell receptor activation. Other mechanisms, such as autophosphorylation of Thr-219, might orchestrate the cellular function of PKC in T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, Thomas -- Freeley, Michael -- Thuille, Nikolaus -- Heit, Isabelle -- Shaw, Stephen -- Long, Aideen -- Baier, Gottfried -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):55; author reply 55.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department for Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601177" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Animals ; Antibodies/immunology ; Antigens, CD28/immunology ; Antigens, CD3/immunology ; Cells, Cultured ; Humans ; Isoenzymes/*metabolism ; Jurkat Cells ; Lymphocyte Activation ; Mice ; NF-kappa B/*metabolism ; Phosphorylation ; Protein Kinase C/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/enzymology/immunology/*metabolism ; Threonine/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 44
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    Hierarchical action and inhibition of plant Dicer-like proteins in antiviral defense (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-03
    Description: The mechanisms underlying induction and suppression of RNA silencing in the ongoing plant-virus arms race are poorly understood. We show here that virus-derived small RNAs produced by Arabidopsis Dicer-like 4 (DCL4) program an effector complex conferring antiviral immunity. Inhibition of DCL4 by a viral-encoded suppressor revealed the subordinate antiviral activity of DCL2. Accordingly, inactivating both DCL2 and DCL4 was necessary and sufficient to restore systemic infection of a suppressor-deficient virus. The effects of DCL2 were overcome by increasing viral dosage in inoculated leaves, but this could not surmount additional, non-cell autonomous effects of DCL4 specifically preventing viral unloading from the vasculature. These findings define a molecular framework for studying antiviral silencing and defense in plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deleris, Angelique -- Gallego-Bartolome, Javier -- Bao, Jinsong -- Kasschau, Kristin D -- Carrington, James C -- Voinnet, Olivier -- AI43288/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):68-71. Epub 2006 Jun 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie Moleculaire des Plantes, CNRS Unite Propre de Recherche (UPR) 2357, 12, rue du General Zimmer, 67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741077" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/enzymology/genetics/metabolism/*virology ; Arabidopsis Proteins/antagonists & inhibitors/genetics/*metabolism ; Carmovirus/physiology ; Cell Cycle Proteins/antagonists & inhibitors/genetics/*metabolism ; Green Fluorescent Proteins/metabolism ; Mutation ; Plant Diseases/virology ; Plant Leaves/virology ; Plant Viruses/*physiology ; Plants, Genetically Modified ; *RNA Interference ; RNA Viruses/physiology ; RNA, Double-Stranded/metabolism ; RNA, Small Interfering/*metabolism ; RNA, Viral/*metabolism ; RNA-Induced Silencing Complex/metabolism ; Recombinant Fusion Proteins/metabolism ; Ribonuclease III/antagonists & inhibitors/genetics/*metabolism ; Ribonucleases/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction ; Viral Proteins/*metabolism
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    Cell biology. Stressed cells cope with protein overload (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ron, David -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):52-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA. ron@saturn.med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cytosol/metabolism ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/genetics/metabolism ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/chemistry/genetics/*metabolism ; Evolution, Molecular ; Gene Expression Regulation ; Membrane Proteins/chemistry/genetics/*metabolism ; Models, Biological ; Protein Biosynthesis ; *Protein Folding ; Protein Sorting Signals/physiology ; Protein Structure, Tertiary ; *RNA Stability ; RNA, Messenger/genetics/*metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic
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    Herpes simplex virus encephalitis in human UNC-93B deficiency (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: Herpes simplex virus-1 (HSV-1) encephalitis (HSE) is the most common form of sporadic viral encephalitis in western countries. Its pathogenesis remains unclear, as it affects otherwise healthy patients and only a small minority of HSV-1-infected individuals. Here, we elucidate a genetic etiology for HSE in two children with autosomal recessive deficiency in the intracellular protein UNC-93B, resulting in impaired cellular interferon-alpha/beta and -lambda antiviral responses. HSE can result from a single-gene immunodeficiency that does not compromise immunity to most pathogens, unlike most known primary immunodeficiencies. Other severe infectious diseases may also reflect monogenic disorders of immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casrouge, Armanda -- Zhang, Shen-Ying -- Eidenschenk, Celine -- Jouanguy, Emmanuelle -- Puel, Anne -- Yang, Kun -- Alcais, Alexandre -- Picard, Capucine -- Mahfoufi, Nora -- Nicolas, Nathalie -- Lorenzo, Lazaro -- Plancoulaine, Sabine -- Senechal, Brigitte -- Geissmann, Frederic -- Tabeta, Koichi -- Hoebe, Kasper -- Du, Xin -- Miller, Richard L -- Heron, Benedicte -- Mignot, Cyril -- de Villemeur, Thierry Billette -- Lebon, Pierre -- Dulac, Olivier -- Rozenberg, Flore -- Beutler, Bruce -- Tardieu, Marc -- Abel, Laurent -- Casanova, Jean-Laurent -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):308-12. Epub 2006 Sep 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Humaine des Maladies Infectieuses, Universite de Paris Rene Descartes, INSERM, U550, Faculte de Medecine Necker, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973841" target="_blank"〉PubMed〈/a〉
    Keywords: Child, Preschool ; Cytokines/biosynthesis ; Encephalitis, Herpes Simplex/*genetics/immunology ; Female ; *Genetic Predisposition to Disease ; *Herpesvirus 1, Human/immunology ; Humans ; Infant ; Interferon-alpha/biosynthesis/immunology ; Interferon-beta/biosynthesis/immunology ; Interferon-gamma/biosynthesis/immunology ; Interferons/*biosynthesis/immunology ; Leukocytes, Mononuclear/immunology ; Male ; Membrane Transport Proteins/*deficiency/genetics/*physiology ; Mutation ; Pedigree ; Signal Transduction ; Toll-Like Receptor 3/agonists/physiology ; Toll-Like Receptors/agonists/physiology
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    Cell signaling. Protein kinases seek close encounters with active genes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edmunds, John W -- Mahadevan, Louis C -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):449-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nuclear Signalling Laboratory, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873633" target="_blank"〉PubMed〈/a〉
    Keywords: Catalytic Domain ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; *Gene Expression Regulation, Fungal ; *Genes, Fungal ; Histones/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/*metabolism ; Oligonucleotide Array Sequence Analysis ; Osmotic Pressure ; Promoter Regions, Genetic ; Protein Binding ; RNA Polymerase II/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic
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    PI(3,4,5)P3 and PI(4,5)P2 lipids target proteins with polybasic clusters to the plasma membrane (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-11
    Description: Many signaling, cytoskeletal, and transport proteins have to be localized to the plasma membrane (PM) in order to carry out their function. We surveyed PM-targeting mechanisms by imaging the subcellular localization of 125 fluorescent protein-conjugated Ras, Rab, Arf, and Rho proteins. Out of 48 proteins that were PM-localized, 37 contained clusters of positively charged amino acids. To test whether these polybasic clusters bind negatively charged phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] lipids, we developed a chemical phosphatase activation method to deplete PM PI(4,5)P2. Unexpectedly, proteins with polybasic clusters dissociated from the PM only when both PI(4,5)P2 and phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P3] were depleted, arguing that both lipid second messengers jointly regulate PM targeting.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579512/" 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/PMC3579512/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heo, Won Do -- Inoue, Takanari -- Park, Wei Sun -- Kim, Man Lyang -- Park, Byung Ouk -- Wandless, Thomas J -- Meyer, Tobias -- R01 GM030179/GM/NIGMS NIH HHS/ -- R01 GM030179-24A1/GM/NIGMS NIH HHS/ -- R01 GM030179-25/GM/NIGMS NIH HHS/ -- R01 GM063702/GM/NIGMS NIH HHS/ -- R01 MH064801/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1458-61. Epub 2006 Nov 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, 318 Campus Drive, Clark Building, Stanford University Medical School, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095657" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factors/chemistry/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Membrane/*metabolism ; GTP Phosphohydrolases/chemistry/*metabolism ; HeLa Cells ; Humans ; Hydrophobic and Hydrophilic Interactions ; Kinetics ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphatidylinositol Phosphates/*metabolism ; Second Messenger Systems ; Signal Transduction ; Static Electricity ; rab GTP-Binding Proteins/chemistry/metabolism ; ras Proteins/chemistry/metabolism ; rho GTP-Binding Proteins/metabolism
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    Gene regulatory networks in the evolution and development of the heart (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: The heart, an ancient organ and the first to form and function during embryogenesis, evolved by the addition of new structures and functions to a primitive pump. Heart development is controlled by an evolutionarily conserved network of transcription factors that connect signaling pathways with genes for muscle growth, patterning, and contractility. During evolution, this ancestral gene network was expanded through gene duplication and co-option of additional networks. Mutations in components of the cardiac gene network cause congenital heart disease, the most common human birth defect. The consequences of such mutations reveal the logic of organogenesis and the evolutionary origins of morphological complexity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459601/" 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/PMC4459601/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Eric N -- P01 HL049953/HL/NHLBI NIH HHS/ -- R01 HL053351/HL/NHLBI NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1922-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila/embryology/genetics ; Gene Duplication ; *Gene Expression Regulation, Developmental ; *Heart/anatomy & histology/embryology/physiology ; Heart Defects, Congenital/genetics/physiopathology ; Humans ; Morphogenesis/genetics ; Mutation ; Regulatory Sequences, Nucleic Acid ; Signal Transduction ; Transcription Factors/genetics/physiology ; Vertebrates/embryology/genetics
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    Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alpha (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: Accumulation of misfolded protein in the endoplasmic reticulum (ER) triggers an adaptive stress response-termed the unfolded protein response (UPR)-mediated by the ER transmembrane protein kinase and endoribonuclease inositol-requiring enzyme-1alpha (IRE1alpha). We investigated UPR signaling events in mice in the absence of the proapoptotic BCL-2 family members BAX and BAK [double knockout (DKO)]. DKO mice responded abnormally to tunicamycin-induced ER stress in the liver, with extensive tissue damage and decreased expression of the IRE1 substrate X-box-binding protein 1 and its target genes. ER-stressed DKO cells showed deficient IRE1alpha signaling. BAX and BAK formed a protein complex with the cytosolic domain of IRE1alpha that was essential for IRE1alpha activation. Thus, BAX and BAK function at the ER membrane to activate IRE1alpha signaling and to provide a physical link between members of the core apoptotic pathway and the UPR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hetz, Claudio -- Bernasconi, Paula -- Fisher, Jill -- Lee, Ann-Hwee -- Bassik, Michael C -- Antonsson, Bruno -- Brandt, Gabriel S -- Iwakoshi, Neal N -- Schinzel, Anna -- Glimcher, Laurie H -- Korsmeyer, Stanley J -- CA100707/CA/NCI NIH HHS/ -- P01 AI56296/AI/NIAID NIH HHS/ -- P01 CA92625/CA/NCI NIH HHS/ -- R01 AI32412/AI/NIAID NIH HHS/ -- R37 CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):572-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA. chetz@hsph.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645094" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; DNA-Binding Proteins/metabolism ; Endoplasmic Reticulum/*metabolism/ultrastructure ; Endoribonucleases/*metabolism ; Gene Expression Regulation ; Heat-Shock Proteins/metabolism ; Humans ; Kidney/cytology/drug effects/metabolism ; Liver/cytology/drug effects/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Molecular Chaperones/metabolism ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Folding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Transcription Factor CHOP/metabolism ; Transcription Factors ; Tunicamycin/pharmacology ; bcl-2 Homologous Antagonist-Killer Protein/chemistry/genetics/*metabolism ; bcl-2-Associated X Protein/genetics/*metabolism ; eIF-2 Kinase/metabolism
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    Reversal of the TCR stop signal by CTLA-4 (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: The coreceptor cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is pivotal in regulating the threshold of signals during T cell activation, although the underlying mechanism is still not fully understood. Using in vitro migration assays and in vivo two-photon laser scanning microscopy, we showed that CTLA-4 increases T cell motility and overrides the T cell receptor (TCR)-induced stop signal required for stable conjugate formation between T cells and antigen-presenting cells. This event led to reduced contact periods between T cells and antigen-presenting cells that in turn decreased cytokine production and proliferation. These results suggest a fundamentally different model of reverse stop signaling, by which CTLA-4 modulates the threshold for T cell activation and protects against autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, Helga -- Downey, Jos -- Smith, Andrew -- Zinselmeyer, Bernd H -- Rush, Catherine -- Brewer, James M -- Wei, Bin -- Hogg, Nancy -- Garside, Paul -- Rudd, Christopher E -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1972-5. Epub 2006 Aug 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Signalling Section, Division of Immunology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD ; Antigens, Differentiation/genetics/*physiology ; Autoimmunity ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology/physiology ; CTLA-4 Antigen ; Cell Adhesion ; Cell Movement ; Dendritic Cells/*immunology ; Humans ; Intercellular Adhesion Molecule-1 ; Lymph Nodes/*immunology ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*physiology ; Transfection
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    Chemical chaperones reduce ER stress and restore glucose homeostasis in a mouse model of type 2 diabetes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: Endoplasmic reticulum (ER) stress is a key link between obesity, insulin resistance, and type 2 diabetes. Here, we provide evidence that this mechanistic link can be exploited for therapeutic purposes with orally active chemical chaperones. 4-Phenyl butyric acid and taurine-conjugated ursodeoxycholic acid alleviated ER stress in cells and whole animals. Treatment of obese and diabetic mice with these compounds resulted in normalization of hyperglycemia, restoration of systemic insulin sensitivity, resolution of fatty liver disease, and enhancement of insulin action in liver, muscle, and adipose tissues. Our results demonstrate that chemical chaperones enhance the adaptive capacity of the ER and act as potent antidiabetic modalities with potential application in the treatment of type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741373/" 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/PMC4741373/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozcan, Umut -- Yilmaz, Erkan -- Ozcan, Lale -- Furuhashi, Masato -- Vaillancourt, Eric -- Smith, Ross O -- Gorgun, Cem Z -- Hotamisligil, Gokhan S -- DK52539/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-11/DK/NIDDK NIH HHS/ -- R01 DK052539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1137-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931765" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Blood Glucose/metabolism ; Cell Line, Tumor ; Diabetes Mellitus, Type 2/drug therapy/*metabolism ; Disease Models, Animal ; Endoplasmic Reticulum/drug effects/*metabolism ; Enzyme Activation ; Eukaryotic Initiation Factor-2/metabolism ; Glucose/administration & dosage/*metabolism ; Glucose Tolerance Test ; Homeostasis ; Insulin/blood/pharmacology ; Insulin Resistance ; JNK Mitogen-Activated Protein Kinases/metabolism ; Liver/metabolism ; Mice ; Mice, Obese ; Phenylbutyrates/*pharmacology/therapeutic use ; Phosphorylation ; Receptor, Insulin/metabolism ; Signal Transduction ; Taurochenodeoxycholic Acid/*pharmacology/therapeutic use ; eIF-2 Kinase/metabolism
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    Cell biology. A stressful situation (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-09-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1564-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973855" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 6/metabolism ; Animals ; DNA-Binding Proteins/metabolism ; Diabetes Mellitus, Type 2/etiology/*physiopathology ; Endoplasmic Reticulum/*physiology ; Gene Expression Regulation ; Humans ; Membrane Glycoproteins/metabolism ; Neoplasms/pathology/*physiopathology ; Neurodegenerative Diseases/*physiopathology ; Nuclear Proteins/metabolism ; Protein Biosynthesis ; *Protein Folding ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/chemistry/*metabolism ; RNA Splicing ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction ; Transcription Factors ; eIF-2 Kinase/metabolism
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    Maternal oxytocin triggers a transient inhibitory switch in GABA signaling in the fetal brain during delivery (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-16
    Description: We report a signaling mechanism in rats between mother and fetus aimed at preparing fetal neurons for delivery. In immature neurons, gamma-aminobutyric acid (GABA) is the primary excitatory neurotransmitter. We found that, shortly before delivery, there is a transient reduction in the intracellular chloride concentration and an excitatory-to-inhibitory switch of GABA actions. These events were triggered by oxytocin, an essential maternal hormone for labor. In vivo administration of an oxytocin receptor antagonist before delivery prevented the switch of GABA actions in fetal neurons and aggravated the severity of anoxic episodes. Thus, maternal oxytocin inhibits fetal neurons and increases their resistance to insults during delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyzio, Roman -- Cossart, Rosa -- Khalilov, Ilgam -- Minlebaev, Marat -- Hubner, Christian A -- Represa, Alfonso -- Ben-Ari, Yehezkel -- Khazipov, Rustem -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1788-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Neurobiologie de la Mediterranee, INSERM U29, Universite de la Mediterranee, Campus Scientifique de Luminy, Boite Postale 13, 13273 Marseille Cedex 09, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170309" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Animals, Newborn ; Benzamides/pharmacology ; Chlorides/metabolism ; Female ; Fetal Hypoxia/physiopathology ; Fetus/*physiology ; GABA-A Receptor Agonists ; GABA-A Receptor Antagonists ; Hippocampus/cytology/*embryology/physiology ; In Vitro Techniques ; Indoles/pharmacology ; Maternal-Fetal Exchange ; *Neural Inhibition ; Neurons/*physiology ; Oxytocin/pharmacology/*physiology ; *Parturition ; Patch-Clamp Techniques ; Pregnancy ; Rats ; Rats, Wistar ; Receptors, GABA-A/physiology ; Receptors, Oxytocin/antagonists & inhibitors ; Signal Transduction ; Sodium Potassium Chloride Symporter Inhibitors ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Vasotocin/analogs & derivatives/pharmacology ; gamma-Aminobutyric Acid/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 55
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    Cell biology. The stress of finding NEMO (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bartek, Jiri -- Lukas, Jiri -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1110-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. jb@cancer.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497923" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Death ; Cell Nucleus/metabolism ; Cell Survival ; Cytoplasm/metabolism ; *DNA Damage ; DNA Repair ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; I-kappa B Kinase/*metabolism ; Models, Biological ; NF-kappa B/metabolism ; Neoplasms/pathology/physiopathology ; Protein-Serine-Threonine Kinases/*metabolism ; SUMO-1 Protein/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin/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)
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  • 56
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    Opposing activities protect against age-onset proteotoxicity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: Aberrant protein aggregation is a common feature of late-onset neurodegenerative diseases, including Alzheimer's disease, which is associated with the misassembly of the Abeta(1-42) peptide. Aggregation-mediated Abeta(1-42) toxicity was reduced in Caenorhabditis elegans when aging was slowed by decreased insulin/insulin growth factor-1-like signaling (IIS). The downstream transcription factors, heat shock factor 1, and DAF-16 regulate opposing disaggregation and aggregation activities to promote cellular survival in response to constitutive toxic protein aggregation. Because the IIS pathway is central to the regulation of longevity and youthfulness in worms, flies, and mammals, these results suggest a mechanistic link between the aging process and aggregation-mediated proteotoxicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Ehud -- Bieschke, Jan -- Perciavalle, Rhonda M -- Kelly, Jeffery W -- Dillin, Andrew -- DK 46335/DK/NIDDK NIH HHS/ -- NS 50636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1604-10. Epub 2006 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, 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/16902091" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Amyloid beta-Peptides/chemistry/*metabolism ; Animals ; Biopolymers/chemistry/metabolism ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Survival ; Forkhead Transcription Factors ; Humans ; Insulin-Like Growth Factor I/metabolism ; Models, Biological ; Molecular Weight ; Movement ; Muscles/metabolism/physiology ; PC12 Cells ; Peptide Fragments/chemistry/*metabolism ; RNA Interference ; Rats ; Receptor, Insulin/genetics/metabolism ; 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)
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  • 57
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    Neuroscience. A new molecule to brighten the mood (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharp, Trevor -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):45-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK. trevor.sharp@pharm.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400139" target="_blank"〉PubMed〈/a〉
    Keywords: Affect/physiology ; Animals ; Annexin A2/genetics/*metabolism ; Antidepressive Agents/pharmacology ; Brain/drug effects/metabolism ; Cell Membrane/metabolism ; Depression/genetics/*metabolism ; Humans ; Mice ; Mice, Knockout ; Receptor, Serotonin, 5-HT1B/*metabolism ; S100 Proteins/genetics/*metabolism ; Serotonin/metabolism ; Signal Transduction ; 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)
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