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  • Signal Transduction  (353)
  • American Association for the Advancement of Science (AAAS)  (353)
  • PANGAEA
  • Periodicals Archive Online (PAO)
  • 2005-2009  (348)
  • 1985-1989  (5)
  • 1980-1984
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  • 1
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    In vivo modulation of cytolytic activity and Thy-1 expression in TCR-gamma delta+ intraepithelial lymphocytes (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-31
    Description: Although the functional aspects of the alpha beta T cell antigen receptor (TCR) found on most peripheral T cells are well described, the function of the gamma delta TCR remains unclear. Murine intraepithelial lymphocytes (IEL) of the small intestine are CD8+, express the gamma delta TCR, and are constitutively lytic. Fresh IEL from germ-free mice had no lytic activity. Moreover, whereas IEL from normal mice are 30 to 50 percent Thy-1+, IEL from germ-free did not express Thy-1. Acclimation of germ-free mice to nonsterile conditions resulted in the generation of Thy-1+ IEL and induction of lytic activity. Thus CD8+ TCR-gamma delta IEL were regulated by externally derived stimuli via a specific functional interaction between IEL and gut-associated antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lefrancois, L -- Goodman, T -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1716-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Upjohn Company, Kalamazoo, MI 49001.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2564701" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/analysis ; Antigens, Surface/*analysis/immunology ; Antigens, Thy-1 ; *Cytotoxicity, Immunologic ; Epithelial Cells ; Germ-Free Life ; Immunosorbent Techniques ; Intestine, Small/*cytology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/analysis/*immunology ; Signal Transduction ; T-Lymphocytes/*immunology
    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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    Beta-adrenergic inhibition of cardiac sodium channels by dual G-protein pathways (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-04
    Description: The signaling pathways by which beta-adrenergic agonists modulate voltage-dependent cardiac sodium currents are unknown, although it is likely that adenosine 3'5'-monophosphate (cAMP) is involved. Single-channel and whole-cell sodium currents were measured in cardiac myocytes and the signal transducing G protein Gs was found to couple beta-adrenergic receptors to sodium channels by both cytoplasmic (indirect) and membrane-delimited (direct) pathways. Hence, Gs can act on at least three effectors in the heart: sodium channels, calcium channels, and adenylyl cyclase. The effect on sodium currents was inhibitory and was enhanced by membrane depolarization. During myocardial ischemia the sodium currents of depolarized cells may be further inhibited by the accompanying increase in catecholamine levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schubert, B -- VanDongen, A M -- Kirsch, G E -- Brown, A M -- DK19319/DK/NIDDK NIH HHS/ -- HL36930/HL/NHLBI NIH HHS/ -- HL39262/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):516-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2547248" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Cyclic AMP/physiology ; Electric Conductivity ; GTP-Binding Proteins/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Triphosphate/analogs & derivatives/pharmacology ; Heart/drug effects/*physiology ; Isoproterenol/pharmacology ; Potassium Channels/physiology ; Rats ; Receptors, Adrenergic, beta/*physiology ; Signal Transduction ; Sodium Channels/*physiology ; Thionucleotides/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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  • 3
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    Interleukin-2 receptor beta chain gene: generation of three receptor forms by cloned human alpha and beta chain cDNA's (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-05
    Description: Interleukin-2 (IL-2) binds to two distinct receptor molecules, the IL-2 receptor alpha (IL-2R alpha, p55) chain and the newly identified IL-2 receptor beta (IL-2R beta, p70-75) chain. The cDNA encoding the human IL-2R beta chain has now been isolated. The overall primary structure of the IL-2R beta chain shows no apparent homology to other known receptors. Unlike the IL-2R alpha chain, the IL-2R beta chain has a large cytoplasmic region in which a functional domain (or domains) mediating an intracellular signal transduction pathway (or pathways) may be embodied. The cDNA-encoded beta chain binds and internalizes IL-2 when expressed on T lymphoid cells but not fibroblast cells. Furthermore, the cDNA gives rise to the generation of high-affinity IL-2 receptor when co-expressed with the IL-2R alpha chain cDNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatakeyama, M -- Tsudo, M -- Minamoto, S -- Kono, T -- Doi, T -- Miyata, T -- Miyasaka, M -- Taniguchi, T -- New York, N.Y. -- Science. 1989 May 5;244(4904):551-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2785715" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; *Cloning, Molecular ; Cross-Linking Reagents ; DNA/*genetics/isolation & purification ; Fibroblasts/metabolism ; Gene Expression Regulation ; Humans ; Interleukin-2/metabolism ; Leukemia ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Interleukin-2/*genetics/metabolism ; Recombinant Proteins ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Succinimides ; T-Lymphocytes/metabolism ; Transfection ; Tumor Cells, Cultured
    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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    G1 events and regulation of cell proliferation (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-03
    Description: Cells prepare for S phase during the G1 phase of the cell cycle. Cell biological methods have provided knowledge of cycle kinetics and of substages of G1 that are determined by extracellular signals. Through the use of biochemical and molecular biological techniques to study effects of growth factors, oncogenes, and inhibitors, intracellular events during G1 that lead to DNA synthesis are rapidly being discovered. Many cells in vivo are in a quiescent state (G0), with unduplicated DNA. Cells can be activated to reenter the cycle during G1. Similarly, cells in culture can be shifted between G0 and G1. These switches in and out of G1 are the main determinants of post-embryonic cell proliferation rate and are defectively controlled in cancer cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pardee, A B -- 24571/PHS HHS/ -- New York, N.Y. -- Science. 1989 Nov 3;246(4930):603-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2683075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; *Cell Division ; Cell Membrane/physiology ; Cell Nucleus/physiology ; Gene Expression ; Humans ; *Interphase ; Models, Biological ; Neoplasms/pathology ; Signal Transduction
    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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  • 5
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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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
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  • 10
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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
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  • 11
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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
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  • 12
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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
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    A genome-wide association study identifies IL23R as an inflammatory bowel disease gene (2006)
    American Association for the Advancement of Science (AAAS)
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    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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    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
    Print ISSN: 0036-8075
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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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    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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    Volatile signaling in plant-plant interactions: "talking trees" in the genomics era (2006)
    American Association for the Advancement of Science (AAAS)
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    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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    Caveolin-1 is essential for liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The FERONIA receptor-like kinase mediates male-female interactions during pollen tube reception (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: In flowering plants, signaling between the male pollen tube and the synergid cells of the female gametophyte is required for fertilization. In the Arabidopsis thaliana mutant feronia (fer), fertilization is impaired; the pollen tube fails to arrest and thus continues to grow inside the female gametophyte. FER encodes a synergid-expressed, plasma membrane-localized receptor-like kinase. We found that the FER protein accumulates asymmetrically in the synergid membrane at the filiform apparatus. Interspecific crosses using pollen from Arabidopsis lyrata and Cardamine flexuosa on A. thaliana stigmas resulted in a fer-like phenotype that correlates with sequence divergence in the extracellular domain of FER. Our findings show that the female control of pollen tube reception is based on a FER-dependent signaling pathway, which may play a role in reproductive isolation barriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobar-Restrepo, Juan-Miguel -- Huck, Norbert -- Kessler, Sharon -- Gagliardini, Valeria -- Gheyselinck, Jacqueline -- Yang, Wei-Cai -- Grossniklaus, Ueli -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):656-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Biology and Zurich-Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673660" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/enzymology/genetics/*physiology ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Brassicaceae/genetics/physiology ; Cell Membrane/enzymology ; Crosses, Genetic ; Evolution, Molecular ; Flowers/cytology/enzymology/*physiology ; Gene Expression ; Genes, Plant ; Germination ; Ligands ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphotransferases/chemistry/*genetics/*metabolism ; Plant Epidermis/enzymology ; Pollen Tube/growth & development/*physiology ; Recombinant Fusion Proteins/metabolism ; Reproduction ; Seeds/growth & development ; Signal Transduction ; Species Specificity
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    Positive regulation of Itk PH domain function by soluble IP4 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-07
    Description: Pleckstrin homology (PH) domain-mediated protein recruitment to cellular membranes is of paramount importance for signal transduction. The recruitment of many PH domains is controlled through production and turnover of their membrane ligand, phosphatidylinositol 3,4,5-trisphosphate (PIP3). We show that phosphorylation of the second messenger inositol 1,4,5-trisphosphate (IP3) into inositol 1,3,4,5-tetrakisphosphate (IP4) establishes another mode of PH domain regulation through a soluble ligand. At physiological concentrations, IP4 promoted PH domain binding to PIP3. In primary mouse CD4+CD8+ thymocytes, this was required for full activation of the protein tyrosine kinase Itk after T cell receptor engagement. Our data suggest that IP4 establishes a feedback loop of phospholipase C-gamma1 activation through Itk that is essential for T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yina H -- Grasis, Juris A -- Miller, Andrew T -- Xu, Ruo -- Soonthornvacharin, Stephen -- Andreotti, Amy H -- Tsoukas, Constantine D -- Cooke, Michael P -- Sauer, Karsten -- AR048848/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):886-9. Epub 2007 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412921" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; *Amino Acid Motifs ; Animals ; Diglycerides/metabolism ; Feedback, Physiological ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol Phosphates/*metabolism/pharmacology ; Lymphopoiesis ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Organ Culture Techniques ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C gamma/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/chemistry/*metabolism ; Receptors, Antigen, T-Cell/immunology ; Second Messenger Systems ; Signal Transduction ; Solubility ; T-Lymphocytes/cytology/immunology/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Forces and bond dynamics in cell adhesion (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: Adhesion of a biological cell to another cell or the extracellular matrix involves complex couplings between cell biochemistry, structural mechanics, and surface bonding. The interactions are dynamic and act through association and dissociation of bonds between very large molecules at rates that change considerably under stress. Combining molecular cell biology with single-molecule force spectroscopy provides a powerful tool for exploring the complexity of cell adhesion, that is, how cell signaling processes strengthen adhesion bonds and how forces applied to cell-surface bonds act on intracellular sites to catalyze chemical processes or switch molecular interactions on and off. Probing adhesion receptors on strategically engineered cells with force during functional stimulation can reveal key nodes of communication between the mechanical and chemical circuitry of a cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evans, Evan A -- Calderwood, David A -- New York, N.Y. -- Science. 2007 May 25;316(5828):1148-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA. evans@physics.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525329" target="_blank"〉PubMed〈/a〉
    Keywords: Biomechanical Phenomena ; Cell Adhesion/*physiology ; Humans ; Integrins/chemistry/physiology ; Selectins/chemistry/physiology ; Signal Transduction ; Spectrum Analysis
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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)
    Details
    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
    Print ISSN: 0036-8075
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    Plant science. Reproductive dialog (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCormick, Sheila -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):606-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Gene Expression Center, USDA Agricultural Research Service-UC Berkeley, 800 Buchanan Street, Albany, CA 94710, USA. sheilamc@nature.berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673644" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/enzymology/genetics/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Cell Membrane/enzymology ; Crosses, Genetic ; Evolution, Molecular ; Flowers/cytology/enzymology/*physiology ; Genes, Plant ; Ligands ; Models, Biological ; Mutation ; Phosphotransferases/*genetics/*metabolism ; Pollen Tube/growth & development/*physiology ; Reproduction ; Signal Transduction ; Species Specificity
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    B cell ligand discrimination through a spreading and contraction response (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Microbiology. Deadly priming (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolter, Roberto -- New York, N.Y. -- Science. 2007 Oct 26;318(5850):578-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115, USA. rkolter@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962544" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Colony Count, Microbial ; Escherichia coli/cytology/*physiology ; Glucosephosphate Dehydrogenase/*metabolism ; Oligopeptides/*metabolism ; *Quorum Sensing ; Signal Transduction
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    Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-31
    Description: Differentiation of hepatic stellate cells (HSCs) to extracellular matrix- and growth factor-producing cells supports liver regeneration through promotion of hepatocyte proliferation. We show that the neurotrophin receptor p75NTR, a tumor necrosis factor receptor superfamily member expressed in HSCs after fibrotic and cirrhotic liver injury in humans, is a regulator of liver repair. In mice, depletion of p75NTR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo. p75NTR-/- HSCs failed to differentiate to myofibroblasts and did not support hepatocyte proliferation. Moreover, inhibition of p75NTR signaling to the small guanosine triphosphatase Rho resulted in impaired HSC differentiation. Our results identify signaling from p75NTR to Rho as a mechanism for the regulation of HSC differentiation to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Passino, Melissa A -- Adams, Ryan A -- Sikorski, Shoana L -- Akassoglou, Katerina -- 5T32-GM07752/GM/NIGMS NIH HHS/ -- NS051470/NS/NINDS NIH HHS/ -- P30-NS047101/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego (UCSD), La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Progression ; Extracellular Matrix/metabolism ; Fibroblasts/*cytology ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/*cytology ; Liver/*cytology/metabolism/pathology/physiology ; Liver Diseases/metabolism/*pathology ; *Liver Regeneration ; Mice ; Nerve Growth Factor/pharmacology ; Receptors, Nerve Growth Factor/genetics/*metabolism ; Signal Transduction ; rho GTP-Binding Proteins/metabolism
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    Genetically determined differences in learning from errors (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-08
    Description: The role of dopamine in monitoring negative action outcomes and feedback-based learning was tested in a neuroimaging study in humans grouped according to the dopamine D2 receptor gene polymorphism DRD2-TAQ-IA. In a probabilistic learning task, A1-allele carriers with reduced dopamine D2 receptor densities learned to avoid actions with negative consequences less efficiently. Their posterior medial frontal cortex (pMFC), involved in feedback monitoring, responded less to negative feedback than others' did. Dynamically changing interactions between pMFC and hippocampus found to underlie feedback-based learning were reduced in A1-allele carriers. This demonstrates that learning from errors requires dopaminergic signaling. Dopamine D2 receptor reduction seems to decrease sensitivity to negative action consequences, which may explain an increased risk of developing addictive behaviors in A1-allele carriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, Tilmann A -- Neumann, Jane -- Reuter, Martin -- Hennig, Jurgen -- von Cramon, D Yves -- Ullsperger, Markus -- R01MH74457/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1642-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany. tklein@cbs.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063800" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alleles ; *Avoidance Learning ; Basal Ganglia/physiology ; Brain Mapping ; Dopamine/*physiology ; Feedback, Psychological ; Frontal Lobe/*physiology ; Hippocampus/physiology ; Humans ; *Learning ; Magnetic Resonance Imaging ; Male ; Nucleus Accumbens/physiology ; *Polymorphism, Genetic ; Receptors, Dopamine D2/*genetics/metabolism ; *Reinforcement (Psychology) ; Signal Transduction
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    Comment on "A centrosome-independent role for gamma-TuRC proteins in the spindle assembly checkpoint" (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-19
    Description: Muller et al. (Reports, 27 October 2006, p. 654) proposed a role for microtubule nucleation in mitotic checkpoint signaling. However, their observations of spindle defects and mitotic delay after depletion of gamma-tubulin ring complex (gamma-TuRC) components are fully consistent with activation of the established pathway of checkpoint signaling in response to incomplete or unstable interactions between kinetochores of mitotic chromosomes and spindle microtubules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weaver, Beth A A -- Cleveland, Don W -- New York, N.Y. -- Science. 2007 May 18;316(5827):982; author reply 982.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and Department of Cellular and Molecular Medicine, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Kinetochores/*physiology ; Microtubule-Associated Proteins/*metabolism ; Microtubules/*metabolism/ultrastructure ; *Mitosis ; Signal Transduction ; Spindle Apparatus/*metabolism ; Tubulin/*metabolism
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    Immunology. The shape of things to come (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fitzgerald, Katherine A -- Golenbock, Douglas T -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1574-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA. kate.fitzgerald@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569850" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Vesicular Transport/metabolism ; *Adjuvants, Immunologic ; Animals ; Crystallography, X-Ray ; Glycolipids/chemistry/metabolism ; Humans ; Hydrophobic and Hydrophilic Interactions ; Ligands ; Lipid A/*analogs & derivatives/chemistry/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Antigen 96/*chemistry/metabolism ; Mice ; Phosphates/metabolism ; Protein Conformation ; Receptors, Interleukin/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/chemistry/*immunology/metabolism
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    Signals from chloroplasts converge to regulate nuclear gene expression (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-31
    Description: Plastid-to-nucleus retrograde signaling coordinates nuclear gene expression with chloroplast function and is essential for the photoautotrophic life-style of plants. Three retrograde signals have been described, but little is known of their signaling pathways. We show here that GUN1, a chloroplast-localized pentatricopeptide-repeat protein, and ABI4, an Apetala 2 (AP2)-type transcription factor, are common to all three pathways. ABI4 binds the promoter of a retrograde-regulated gene through a conserved motif found in close proximity to a light-regulatory element. We propose a model in which multiple indicators of aberrant plastid function in Arabidopsis are integrated upstream of GUN1 within plastids, which leads to ABI4-mediated repression of nuclear-encoded genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koussevitzky, Shai -- Nott, Ajit -- Mockler, Todd C -- Hong, Fangxin -- Sachetto-Martins, Gilberto -- Surpin, Marci -- Lim, Jason -- Mittler, Ron -- Chory, Joanne -- DRG-1865-05/PHS HHS/ -- F32 GM 18172/GM/NIGMS NIH HHS/ -- F32 GM 69090/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 4;316(5825):715-9. Epub 2007 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/17395793" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid ; Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Cell Nucleus/*metabolism/*microbiology ; Chloroplasts/*metabolism ; DNA, Plant/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Electron Transport ; *Gene Expression Regulation, Plant ; Light-Harvesting Protein Complexes/genetics ; Lincomycin/pharmacology ; Models, Biological ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Protoporphyrins/metabolism ; Pyridazines/pharmacology ; Signal Transduction ; Transcription Factors/*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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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
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    The slit receptor EVA-1 coactivates a SAX-3/Robo mediated guidance signal in C. elegans (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-29
    Description: The SAX-3/roundabout (Robo) receptor has SLT-1/Slit-dependent and -independent functions in guiding cell and axon migrations. We identified enhancer of ventral-axon guidance defects of unc-40 mutants (EVA-1) as a Caenorhabditis elegans transmembrane receptor for SLT-1. EVA-1 has two predicted galactose-binding ectodomains, acts cell-autonomously for SLT-1/Slit-dependent axon migration functions of SAX-3/Robo, binds to SLT-1 and SAX-3, colocalizes with SAX-3 on cells, and provides cell specificity to the activation of SAX-3 signaling by SLT-1. Double mutants of eva-1 or slt-1 with sax-3 mutations suggest that SAX-3 can (when slt-1 or eva-1 function is reduced) inhibit a parallel-acting guidance mechanism, which involves UNC-40/deleted in colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisawa, Kazuko -- Wrana, Jeffrey L -- Culotti, Joseph G -- NS41397/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1934-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute of Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Axons/*physiology ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/*chemistry/genetics/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Movement ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/*metabolism ; Nervous System/growth & development/metabolism ; Neurons/physiology ; Protein Structure, Tertiary ; Receptors, Immunologic/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Male and female Drosophila germline stem cells: two versions of immortality (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: Drosophila male and female germline stem cells (GSCs) are sustained by niches and regulatory pathways whose common principles serve as models for understanding mammalian stem cells. Despite striking cellular and genetic similarities that suggest a common evolutionary origin, however, male and female GSCs also display important differences. Comparing these two stem cells and their niches in detail is likely to reveal how a common heritage has been adapted to the differing requirements of male and female gamete production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuller, Margaret T -- Spradling, Allan C -- P01DK53074/DK/NIDDK NIH HHS/ -- R01GM61986/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):402-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446390" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology/physiology ; Animals ; Cell Adhesion ; Cell Differentiation ; Cell Division ; Centrosome/physiology ; Drosophila/*cytology/*physiology ; Drosophila Proteins/physiology ; Female ; Germ Cells/*cytology/physiology ; Male ; Ovary/cytology ; Sex Characteristics ; Signal Transduction ; Testis/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Physiology. An integrative view of obesity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wisse, Brent E -- Kim, Francis -- Schwartz, Michael W -- DK073878/DK/NIDDK NIH HHS/ -- DK12829/DK/NIDDK NIH HHS/ -- DK61384/DK/NIDDK NIH HHS/ -- NS3227/NS/NINDS NIH HHS/ -- P01-DK 068384/DK/NIDDK NIH HHS/ -- R01 DK074758/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):928-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harborview Medical Center and University of Washington, Seattle, WA 98104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991852" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Coenzyme A/metabolism ; Adipose Tissue/metabolism ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Endothelium, Vascular/metabolism ; *Energy Intake ; Energy Metabolism ; Homeostasis ; Humans ; Hypothalamus/metabolism ; Inflammation/metabolism ; Insulin/metabolism/secretion ; Insulin Resistance ; Insulin-Secreting Cells/metabolism ; Leptin/metabolism ; Nitric Oxide/metabolism ; Obesity/etiology/*metabolism ; Oxidative Stress ; Phosphatidylinositol 3-Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Sea anemone genome reveals ancestral eumetazoan gene repertoire and genomic organization (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: Sea anemones are seemingly primitive animals that, along with corals, jellyfish, and hydras, constitute the oldest eumetazoan phylum, the Cnidaria. Here, we report a comparative analysis of the draft genome of an emerging cnidarian model, the starlet sea anemone Nematostella vectensis. The sea anemone genome is complex, with a gene repertoire, exon-intron structure, and large-scale gene linkage more similar to vertebrates than to flies or nematodes, implying that the genome of the eumetazoan ancestor was similarly complex. Nearly one-fifth of the inferred genes of the ancestor are eumetazoan novelties, which are enriched for animal functions like cell signaling, adhesion, and synaptic transmission. Analysis of diverse pathways suggests that these gene "inventions" along the lineage leading to animals were likely already well integrated with preexisting eukaryotic genes in the eumetazoan progenitor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putnam, Nicholas H -- Srivastava, Mansi -- Hellsten, Uffe -- Dirks, Bill -- Chapman, Jarrod -- Salamov, Asaf -- Terry, Astrid -- Shapiro, Harris -- Lindquist, Erika -- Kapitonov, Vladimir V -- Jurka, Jerzy -- Genikhovich, Grigory -- Grigoriev, Igor V -- Lucas, Susan M -- Steele, Robert E -- Finnerty, John R -- Technau, Ulrich -- Martindale, Mark Q -- Rokhsar, Daniel S -- 5 P41 LM006252-09/LM/NLM NIH HHS/ -- THL007279F/PHS HHS/ -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):86-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cell Adhesion ; Evolution, Molecular ; Genes ; Genetic Linkage ; *Genome ; Genome, Human ; Genomics ; Humans ; Introns ; Metabolic Networks and Pathways ; Multigene Family ; Muscles/physiology ; Nervous System Physiological Phenomena ; Phylogeny ; Sea Anemones/*genetics/metabolism ; Sequence Analysis, DNA ; Signal Transduction ; Synteny
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    Of aging mice and men (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Richard -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):390; author reply 390.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947563" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Glucuronidase/deficiency/*genetics ; Humans ; Mice ; *Models, Animal ; Signal Transduction ; Vitamin D/*administration & dosage/metabolism ; Wnt Proteins/metabolism
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    Demethylation of H3K27 regulates polycomb recruitment and H2A ubiquitination (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: Methylation of histone H3 lysine 27 (H3K27) is a posttranslational modification that is highly correlated with genomic silencing. Here we show that human UTX, a member of the Jumonji C family of proteins, is a di- and trimethyl H3K27 demethylase. UTX occupies the promoters of HOX gene clusters and regulates their transcriptional output by modulating the recruitment of polycomb repressive complex 1 and the monoubiquitination of histone H2A. Moreover, UTX associates with mixed-lineage leukemia (MLL) 2/3 complexes, and during retinoic acid signaling events, the recruitment of the UTX complex to HOX genes results in H3K27 demethylation and a concomitant methylation of H3K4. Our results suggest a concerted mechanism for transcriptional activation in which cycles of H3K4 methylation by MLL2/3 are linked with the demethylation of H3K27 through UTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Min Gyu -- Villa, Raffaella -- Trojer, Patrick -- Norman, Jessica -- Yan, Kai-Ping -- Reinberg, Danny -- Di Croce, Luciano -- Shiekhattar, Ramin -- R01CA090758/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):447-50. Epub 2007 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761849" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Line ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells ; *Genes, Homeobox ; Histone Demethylases ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Methylation ; Multigene Family ; Neoplasm Proteins/metabolism ; Nuclear Proteins/genetics/*metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism ; Repressor Proteins/*metabolism ; Signal Transduction ; Transcription, Genetic ; Transcriptional Activation ; Tretinoin/metabolism/pharmacology ; Ubiquitin/metabolism
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    Immunology. Eating in to avoid infection (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1376-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. caetano@cancer.org.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cytokines/metabolism ; Dendritic Cells/*immunology/physiology/*virology ; Endosomes/immunology/virology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Membrane Glycoproteins/immunology/physiology ; Mice ; Mice, Transgenic ; RNA, Viral/*immunology/metabolism ; Rhabdoviridae Infections/*immunology ; Signal Transduction ; Toll-Like Receptor 7/immunology/physiology ; Toll-Like Receptor 9/immunology/physiology ; Toll-Like Receptors/immunology/*physiology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Virus Replication
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    Biochemistry. Signaling across the cell membrane (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ranganathan, Rama -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1253-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Green Center for Systems Biology and Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. rama.ranganathan@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033872" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/chemistry/metabolism ; Adrenergic beta-Antagonists/chemistry/metabolism/pharmacology ; Bacteriophage T4/enzymology ; Binding Sites ; Cell Membrane/chemistry/metabolism ; Immunoglobulin Fab Fragments/metabolism ; Ligands ; Muramidase/chemistry/metabolism ; Propanolamines/chemistry/metabolism ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Receptors, Adrenergic, beta-2/*chemistry/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Rhodopsin/chemistry/metabolism ; Signal Transduction
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    Legumes symbioses: absence of Nod genes in photosynthetic bradyrhizobia (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-02
    Description: Leguminous plants (such as peas and soybeans) and rhizobial soil bacteria are symbiotic partners that communicate through molecular signaling pathways, resulting in the formation of nodules on legume roots and occasionally stems that house nitrogen-fixing bacteria. Nodule formation has been assumed to be exclusively initiated by the binding of bacterial, host-specific lipochito-oligosaccharidic Nod factors, encoded by the nodABC genes, to kinase-like receptors of the plant. Here we show by complete genome sequencing of two symbiotic, photosynthetic, Bradyrhizobium strains, BTAi1 and ORS278, that canonical nodABC genes and typical lipochito-oligosaccharidic Nod factors are not required for symbiosis in some legumes. Mutational analyses indicated that these unique rhizobia use an alternative pathway to initiate symbioses, where a purine derivative may play a key role in triggering nodule formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giraud, Eric -- Moulin, Lionel -- Vallenet, David -- Barbe, Valerie -- Cytryn, Eddie -- Avarre, Jean-Christophe -- Jaubert, Marianne -- Simon, Damien -- Cartieaux, Fabienne -- Prin, Yves -- Bena, Gilles -- Hannibal, Laure -- Fardoux, Joel -- Kojadinovic, Mila -- Vuillet, Laurie -- Lajus, Aurelie -- Cruveiller, Stephane -- Rouy, Zoe -- Mangenot, Sophie -- Segurens, Beatrice -- Dossat, Carole -- Franck, William L -- Chang, Woo-Suk -- Saunders, Elizabeth -- Bruce, David -- Richardson, Paul -- Normand, Philippe -- Dreyfus, Bernard -- Pignol, David -- Stacey, Gary -- Emerich, David -- Vermeglio, Andre -- Medigue, Claudine -- Sadowsky, Michael -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1307-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Recherche pour le Developpement, Centre de Cooperation International en Recherche Agronomique pour le Developpement, Institut National de la Recherche Agronomique, Universite Montpellier 2, France. giraud@mpl.ird.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540897" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Amidohydrolases/genetics/metabolism ; Bacterial Proteins/genetics/metabolism ; Bradyrhizobium/*genetics/growth & development/*physiology ; Cytokinins/metabolism ; Fabaceae/*microbiology ; Genes, Bacterial ; Genome, Bacterial ; Genomics ; Lipopolysaccharides/metabolism ; Molecular Sequence Data ; Mutation ; N-Acetylglucosaminyltransferases/genetics/metabolism ; Photosynthesis ; Plant Roots/microbiology ; Plant Stems/*microbiology ; Purines/biosynthesis ; Root Nodules, Plant/microbiology/*physiology ; Signal Transduction ; *Symbiosis
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    DUBA: a deubiquitinase that regulates type I interferon production (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-10
    Description: Production of type I interferon (IFN-I) is a critical host defense triggered by pattern-recognition receptors (PRRs) of the innate immune system. Deubiquitinating enzyme A (DUBA), an ovarian tumor domain-containing deubiquitinating enzyme, was discovered in a small interfering RNA-based screen as a regulator of IFN-I production. Reduction of DUBA augmented the PRR-induced IFN-I response, whereas ectopic expression of DUBA had the converse effect. DUBA bound tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein essential for the IFN-I response. TRAF3 is an E3 ubiquitin ligase that preferentially assembled lysine-63-linked polyubiquitin chains. DUBA selectively cleaved the lysine-63-linked polyubiquitin chains on TRAF3, resulting in its dissociation from the downstream signaling complex containing TANK-binding kinase 1. A discrete ubiquitin interaction motif within DUBA was required for efficient deubiquitination of TRAF3 and optimal suppression of IFN-I. Our data identify DUBA as a negative regulator of innate immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayagaki, Nobuhiko -- Phung, Qui -- Chan, Salina -- Chaudhari, Ruchir -- Quan, Casey -- O'Rourke, Karen M -- Eby, Michael -- Pietras, Eric -- Cheng, Genhong -- Bazan, J Fernando -- Zhang, Zemin -- Arnott, David -- Dixit, Vishva M -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1628-32. Epub 2007 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991829" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Line ; Endopeptidases/*metabolism ; Humans ; Interferon Type I/*biosynthesis/genetics ; Interferon-alpha/genetics ; Molecular Sequence Data ; NF-kappa B/metabolism ; Protein Structure, Tertiary ; RNA, Small Interfering ; Signal Transduction ; TNF Receptor-Associated Factor 3/metabolism ; Toll-Like Receptor 3/metabolism ; Ubiquitin/metabolism ; Ubiquitination
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    Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Targeted therapies that inhibit receptor tyrosine kinases (RTKs) and the downstream phosphatidylinositol 3-kinase (PI3K) signaling pathway have shown promising anticancer activity, but their efficacy in the brain tumor glioblastoma multiforme (GBM) and other solid tumors has been modest. We hypothesized that multiple RTKs are coactivated in these tumors and that redundant inputs drive and maintain downstream signaling, thereby limiting the efficacy of therapies targeting single RTKs. Tumor cell lines, xenotransplants, and primary tumors indeed show multiple concomitantly activated RTKs. Combinations of RTK inhibitors and/or RNA interference, but not single agents, decreased signaling, cell survival, and anchorage-independent growth even in glioma cells deficient in PTEN, a frequently inactivated inhibitor of PI3K. Thus, effective GBM therapy may require combined regimens targeting multiple RTKs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stommel, Jayne M -- Kimmelman, Alec C -- Ying, Haoqiang -- Nabioullin, Roustem -- Ponugoti, Aditya H -- Wiedemeyer, Ruprecht -- Stegh, Alexander H -- Bradner, James E -- Ligon, Keith L -- Brennan, Cameron -- Chin, Lynda -- DePinho, Ronald A -- 5P01CA95616/CA/NCI NIH HHS/ -- R01CA99041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):287-90. Epub 2007 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872411" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology/therapeutic use ; Brain Neoplasms/drug therapy/*enzymology ; Cell Line, Tumor ; Cell Survival ; Enzyme Activation ; Erlotinib Hydrochloride ; Glioblastoma/drug therapy/*enzymology ; Humans ; Indoles/pharmacology ; PTEN Phosphohydrolase/genetics/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Piperazines/pharmacology ; Protein Kinase Inhibitors/*pharmacology ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-met ; Quinazolines/pharmacology ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/metabolism ; Receptors, Growth Factor/metabolism ; Signal Transduction ; Sulfonamides/pharmacology
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    Synchrony dynamics during initiation, failure, and rescue of the segmentation clock (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-19
    Description: The "segmentation clock" is thought to coordinate sequential segmentation of the body axis in vertebrate embryos. This clock comprises a multicellular genetic network of synchronized oscillators, coupled by intercellular Delta-Notch signaling. How this synchrony is established and how its loss determines the position of segmentation defects in Delta and Notch mutants are unknown. We analyzed the clock's synchrony dynamics by varying strength and timing of Notch coupling in zebra-fish embryos with techniques for quantitative perturbation of gene function. We developed a physical theory based on coupled phase oscillators explaining the observed onset and rescue of segmentation defects, the clock's robustness against developmental noise, and a critical point beyond which synchrony decays. We conclude that synchrony among these genetic oscillators can be established by simultaneous initiation and self-organization and that the segmentation defect position is determined by the difference between coupling strength and noise.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riedel-Kruse, Ingmar H -- Muller, Claudia -- Oates, Andrew C -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1911-5. Epub 2007 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), Pfotenhauerstrasse 108, 01307 Dresden, Germany. ingmar@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*genetics/physiology ; *Body Patterning/genetics ; Dipeptides/pharmacology ; Embryo, Nonmammalian/metabolism ; *Embryonic Development ; Gene Expression Regulation, Developmental ; Gene Regulatory Networks ; Homeodomain Proteins/genetics/metabolism ; Intracellular Signaling Peptides and Proteins ; Mathematics ; Membrane Proteins/genetics/metabolism ; Mesoderm/physiology ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Oligonucleotides, Antisense/pharmacology ; RNA Stability ; Receptor, Notch1/genetics/metabolism ; Signal Transduction ; Somites/physiology ; Zebrafish/*embryology/genetics ; Zebrafish Proteins/genetics/*metabolism
    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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    Postreplicative formation of cohesion is required for repair and induced by a single DNA break (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: Sister-chromatid cohesion, established during replication by the protein complex cohesin, is essential for both chromosome segregation and double-strand break (DSB) repair. Normally, cohesion formation is strictly limited to the S phase of the cell cycle, but DSBs can trigger cohesion also after DNA replication has been completed. The function of this damage-induced cohesion remains unknown. In this investigation, we show that damage-induced cohesion is essential for repair in postreplicative cells in yeast. Furthermore, it is established genome-wide after induction of a single DSB, and it is controlled by the DNA damage response and cohesin-regulating factors. We thus define a cohesion establishment pathway that is independent of DNA duplication and acts together with cohesion formed during replication in sister chromatid-based DSB repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strom, Lena -- Karlsson, Charlotte -- Lindroos, Hanna Betts -- Wedahl, Sara -- Katou, Yuki -- Shirahige, Katsuhiko -- Sjogren, Camilla -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Karolinska Institute, 171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626884" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics/metabolism ; Cell Cycle Proteins/metabolism ; Cell Division ; Chromatids/*physiology ; Chromosomal Proteins, Non-Histone/metabolism ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA Replication ; DNA, Fungal/biosynthesis/*metabolism ; G2 Phase ; Genome, Fungal ; Intracellular Signaling Peptides and Proteins ; Mutation ; Nuclear Proteins/genetics/metabolism ; Protein-Serine-Threonine Kinases ; Saccharomyces cerevisiae/genetics/metabolism/*physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Medicine. The yin-yang of sirtuins (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dillin, Andrew -- Kelly, Jeffery W -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):461-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. dillin@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17656709" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autophagy ; Cell Line, Tumor ; Disease Models, Animal ; Drosophila melanogaster ; Humans ; Neurodegenerative Diseases/physiopathology ; Parkinson Disease/drug therapy/pathology/*physiopathology ; RNA Interference ; Rats ; Signal Transduction ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/*antagonists & inhibitors/genetics/metabolism/*physiology ; Transfection ; alpha-Synuclein/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Comment on "A centrosome-independent role for gamma-TuRC proteins in the spindle assembly checkpoint" (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: Muller et al. (Reports, 27 October 2006, p. 654) showed that inhibition of the gamma-tubulin ring complex (gamma-TuRC) activates the spindle assembly checkpoint (SAC), which led them to suggest that gamma-TuRC proteins play molecular roles in SAC activation. Because gamma-TuRC inhibition leads to pleiotropic spindle defects, which are well known to activate kinetochore-derived checkpoint signaling, we believe that this conclusion is premature.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590763/" 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/PMC2590763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, Stephen S -- Hardwick, Kevin G -- Sawin, Kenneth E -- Biggins, Sue -- Piatti, Simonetta -- Khodjakov, Alexey -- Rieder, Conly L -- Salmon, Edward D -- Musacchio, Andrea -- R01 GM059363/GM/NIGMS NIH HHS/ -- R01 GM059363-09/GM/NIGMS NIH HHS/ -- R37 GM040198/GM/NIGMS NIH HHS/ -- R37 GM040198-23/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 18;316(5827):982; author reply 982.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Life Sciences, University of Manchester, Manchester, UK. stephen.taylor@manchester.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Centrosome/physiology ; Kinetochores/*physiology ; Microtubule-Associated Proteins/antagonists & inhibitors/*metabolism ; Microtubules/*metabolism/ultrastructure ; *Mitosis ; Signal Transduction ; Spindle Apparatus/*metabolism ; Tubulin/*metabolism
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    Multiple functions of the IKK-related kinase IKKepsilon in interferon-mediated antiviral immunity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: IKKepsilon is an IKK (inhibitor of nuclear factor kappaBkinase)-related kinase implicated in virus induction of interferon-beta (IFNbeta). We report that, although mice lacking IKKepsilon produce normal amounts of IFNbeta, they are hypersusceptible to viral infection because of a defect in the IFN signaling pathway. Specifically, a subset of type I IFN-stimulated genes are not activated in the absence of IKKepsilon because the interferon-stimulated gene factor 3 complex (ISGF3) does not bind to promoter elements of the affected genes. We demonstrate that IKKepsilon is activated by IFNbeta and that IKKepsilon directly phosphorylates signal transducer and activator of transcription 1 (STAT1), a component of ISGF3. We conclude that IKKepsilon plays a critical role in the IFN-inducible antiviral transcriptional response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tenoever, Benjamin R -- Ng, Sze-Ling -- Chua, Mark A -- McWhirter, Sarah M -- Garcia-Sastre, Adolfo -- Maniatis, Tom -- F31 AI056678/AI/NIAID NIH HHS/ -- P01AI058113/AI/NIAID NIH HHS/ -- R01AI46954/AI/NIAID NIH HHS/ -- U19AI62623/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1274-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332413" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/genetics/metabolism ; Animals ; Cells, Cultured ; Dimerization ; *Gene Expression Regulation ; I-kappa B Kinase/genetics/*metabolism ; *Influenza A Virus, H1N1 Subtype/immunology/physiology ; Interferon-Stimulated Gene Factor 3/metabolism ; Interferon-beta/*immunology/metabolism ; Lung/pathology/virology ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/*immunology/metabolism/pathology/virology ; Phosphorylation ; Promoter Regions, Genetic ; RNA-Binding Proteins ; STAT1 Transcription Factor/metabolism ; STAT2 Transcription Factor/metabolism ; Signal Transduction ; Transcription, Genetic ; Viral Load ; Virus Replication
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    Cysteine redox sensor in PKGIa enables oxidant-induced activation (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: Changes in the concentration of oxidants in cells can regulate biochemical signaling mechanisms that control cell function. We have found that guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) functions directly as a redox sensor. The Ialpha isoform, PKGIalpha, formed an interprotein disulfide linking its two subunits in cells exposed to exogenous hydrogen peroxide. This oxidation directly activated the kinase in vitro, and in rat cells and tissues. The affinity of the kinase for substrates it phosphorylates was enhanced by disulfide formation. This oxidation-induced activation represents an alternate mechanism for regulation along with the classical activation involving nitric oxide and cGMP. This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovascular system and provides a molecular explantion for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burgoyne, Joseph R -- Madhani, Melanie -- Cuello, Friederike -- Charles, Rebecca L -- Brennan, Jonathan P -- Schroder, Ewald -- Browning, Darren D -- Eaton, Philip -- G0700320/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1393-7. Epub 2007 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Cardiovascular Division, King's College London, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta ; Cell Line ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/genetics/*metabolism ; Cysteine/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Nitric Oxide/metabolism ; Oxidants/*metabolism ; Oxidation-Reduction ; Oxidative Stress ; Rats ; Rats, Wistar ; Signal Transduction ; Tissue Culture Techniques ; Transfection ; Vasodilation/physiology
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    Combinatorial ShcA docking interactions support diversity in tissue morphogenesis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: Changes in protein-protein interactions may allow polypeptides to perform unexpected regulatory functions. Mammalian ShcA docking proteins have amino-terminal phosphotyrosine (pTyr) binding (PTB) and carboxyl-terminal Src homology 2 (SH2) domains, which recognize specific pTyr sites on activated receptors, and a central region with two phosphorylated tyrosine-X-asparagine (pYXN) motifs (where X represents any amino acid) that each bind the growth factor receptor-bound protein 2 (Grb2) adaptor. Phylogenetic analysis indicates that ShcA may signal through both pYXN-dependent and -independent pathways. We show that, in mice, cardiomyocyte-expressed ShcA directs mid-gestational heart development by a PTB-dependent mechanism that does not require the pYXN motifs. In contrast, the pYXN motifs are required with PTB and SH2 domains in the same ShcA molecule for the formation of muscle spindles, skeletal muscle sensory organs that regulate motor behavior. Thus, combinatorial differences in ShcA docking interactions may yield multiple signaling mechanisms to support diversity in tissue morphogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575375/" 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/PMC2575375/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardy, W Rod -- Li, Lingying -- Wang, Zhi -- Sedy, Jiri -- Fawcett, James -- Frank, Eric -- Kucera, Jan -- Pawson, Tony -- R01 NS024373/NS/NINDS NIH HHS/ -- R01 NS024373-18/NS/NINDS NIH HHS/ -- R01 NS024373-19/NS/NINDS NIH HHS/ -- R01 NS024373-20/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):251-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626887" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/genetics/*metabolism ; Amino Acid Motifs ; Animals ; Ataxia ; Excitatory Postsynaptic Potentials ; Genetic Complementation Test ; Heart/*embryology ; Mice ; Mice, Knockout ; *Morphogenesis ; Motor Activity ; Muscle Spindles/*embryology ; Muscle, Skeletal/*embryology/metabolism ; Mutation ; Myocytes, Cardiac/*metabolism ; Neurons, Afferent/physiology ; Phosphorylation ; Protein Structure, Tertiary ; Shc Signaling Adaptor Proteins ; Signal Transduction ; src Homology Domains
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    Materials science. Polymer therapeutics (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884993/" 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/PMC2884993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kiick, Kristi L -- P20 RR017716/RR/NCRR NIH HHS/ -- P20 RR017716-010004/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1182-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, University of Delaware, Newark, DE 19716, USA. kiick@udel.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761873" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/immunology ; Drug Carriers ; Drug Delivery Systems ; Drug Design ; Hydrogels ; L-Selectin/metabolism ; Leukocytes/metabolism ; Ligands ; Peptides/chemistry/metabolism/*therapeutic use ; Polymers/chemistry/metabolism/*therapeutic use ; Receptors, Antigen, B-Cell/immunology/metabolism ; Receptors, Cell Surface/metabolism ; Signal Transduction
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    Plant science. Infectious heresy (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Downie, J Allan -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1296-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, John Innes Centre, Norwich NR4 7UH, UK. allan.downie@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540893" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Bacterial Proteins/genetics/metabolism ; Bradyrhizobium/genetics/growth & development/*physiology ; Cytokinins/metabolism ; Fabaceae/*microbiology ; Genes, Bacterial ; Mutation ; N-Acetylglucosaminyltransferases/genetics/metabolism ; *Nitrogen Fixation ; Photosynthesis ; Plant Roots/microbiology ; Plant Stems/microbiology ; Purines/biosynthesis ; Root Nodules, Plant/microbiology/*physiology ; Signal Transduction ; *Symbiosis
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    Asymmetric T lymphocyte division in the initiation of adaptive immune responses (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: A hallmark of mammalian immunity is the heterogeneity of cell fate that exists among pathogen-experienced lymphocytes. We show that a dividing T lymphocyte initially responding to a microbe exhibits unequal partitioning of proteins that mediate signaling, cell fate specification, and asymmetric cell division. Asymmetric segregation of determinants appears to be coordinated by prolonged interaction between the T cell and its antigen-presenting cell before division. Additionally, the first two daughter T cells displayed phenotypic and functional indicators of being differentially fated toward effector and memory lineages. These results suggest a mechanism by which a single lymphocyte can apportion diverse cell fates necessary for adaptive immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, John T -- Palanivel, Vikram R -- Kinjyo, Ichiko -- Schambach, Felix -- Intlekofer, Andrew M -- Banerjee, Arnob -- Longworth, Sarah A -- Vinup, Kristine E -- Mrass, Paul -- Oliaro, Jane -- Killeen, Nigel -- Orange, Jordan S -- Russell, Sarah M -- Weninger, Wolfgang -- Reiner, Steven L -- AI007532/AI/NIAID NIH HHS/ -- AI042370/AI/NIAID NIH HHS/ -- AI053827/AI/NIAID NIH HHS/ -- AI055428/AI/NIAID NIH HHS/ -- AI061699/AI/NIAID NIH HHS/ -- AI069380/AI/NIAID NIH HHS/ -- CA114114/CA/NCI NIH HHS/ -- CA87812/CA/NCI NIH HHS/ -- DK007066/DK/NIDDK NIH HHS/ -- GM007170/GM/NIGMS NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1687-91. Epub 2007 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332376" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens, CD/analysis ; Antigens, CD8/analysis ; CD8-Positive T-Lymphocytes/*cytology/*immunology ; Cell Differentiation ; *Cell Division ; Cell Lineage ; Cell Polarity ; Dendritic Cells/immunology ; *Immunologic Memory ; Intracellular Signaling Peptides and Proteins/metabolism ; Listeria monocytogenes/immunology ; Listeriosis/immunology ; Lymphocyte Activation ; Membrane Proteins/analysis ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitosis ; Nerve Tissue Proteins/analysis ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Receptors, Interferon/analysis ; Signal Transduction ; T-Lymphocyte Subsets/*cytology/*immunology ; T-Lymphocytes, Helper-Inducer/immunology
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    Regulation of B versus T lymphoid lineage fate decision by the proto-oncogene LRF (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-15
    Description: Hematopoietic stem cells in the bone marrow give rise to lymphoid progenitors, which subsequently differentiate into B and T lymphocytes. Here we show that the proto-oncogene LRF plays an essential role in the B versus T lymphoid cell-fate decision. We demonstrate that LRF is key for instructing early lymphoid progenitors in mice to develop into B lineage cells by repressing T cell-instructive signals produced by the cell-fate signal protein, Notch. We propose a new model for lymphoid lineage commitment, in which LRF acts as a master regulator of the cell's determination of B versus T lineage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978506/" 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/PMC2978506/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeda, Takahiro -- Merghoub, Taha -- Hobbs, Robin M -- Dong, Lin -- Maeda, Manami -- Zakrzewski, Johannes -- van den Brink, Marcel R M -- Zelent, Arthur -- Shigematsu, Hirokazu -- Akashi, Koichi -- Teruya-Feldstein, Julie -- Cattoretti, Giorgio -- Pandolfi, Pier Paolo -- CA-102142/CA/NCI NIH HHS/ -- R01 CA102142/CA/NCI NIH HHS/ -- R01 CA102142-06A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):860-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17495164" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/physiology ; Bone Marrow Cells/cytology ; Cell Lineage ; Cells, Cultured ; DNA-Binding Proteins/*genetics/physiology ; Gene Deletion ; Hematopoietic Stem Cells/*cytology/physiology ; *Lymphopoiesis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Biological ; *Proto-Oncogenes ; Receptors, Notch/*metabolism ; Signal Transduction ; T-Lymphocytes/*cytology/physiology ; Thymus Gland/cytology ; Transcription Factors/*genetics/physiology
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    Development. Built to run, not fail (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oliveri, Paola -- Davidson, Eric H -- HD-37105/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 16;315(5818):1510-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. poliveri@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17363653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryonic Development/*genetics ; *Gene Regulatory Networks ; Genes, Regulator ; Repressor Proteins/genetics/metabolism ; Signal Transduction ; Transcription Factors/genetics/metabolism
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    Cell biology. Proteins that promote long life (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Stuart K -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):603-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology and Genetics, Stanford University Medical Center, Stanford, CA 94305-5329, USA. kim@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673641" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Gene Expression Regulation ; Genes, Helminth ; Longevity/*physiology ; Mass Spectrometry ; Metabolic Networks and Pathways ; Models, Animal ; Mutation ; RNA Interference ; Receptor, Insulin/genetics/*metabolism ; Signal Transduction
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    Promotion of tissue inflammation by the immune receptor Tim-3 expressed on innate immune cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-17
    Description: CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous pathways, including the negative immune receptor Tim-3. We found that Tim-3 is constitutively expressed on cells of the innate immune system in both mice and humans, and that it can synergize with Toll-like receptors. Moreover, an antibody agonist of Tim-3 acted as an adjuvant during induced immune responses, and Tim-3 ligation induced distinct signaling events in T cells and dendritic cells; the latter finding could explain the apparent divergent functions of Tim-3 in these cell types. Thus, by virtue of differential expression on innate versus adaptive immune cells, Tim-3 can either promote or terminate TH1 immunity and may be able to influence a range of inflammatory conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Ana C -- Anderson, David E -- Bregoli, Lisa -- Hastings, William D -- Kassam, Nasim -- Lei, Charles -- Chandwaskar, Rucha -- Karman, Jozsef -- Su, Ee W -- Hirashima, Mitsuomi -- Bruce, Jeffrey N -- Kane, Lawrence P -- Kuchroo, Vijay K -- Hafler, David A -- R01 AI067544/AI/NIAID NIH HHS/ -- R01 AI067544-01A2/AI/NIAID NIH HHS/ -- R56 AI067544/AI/NIAID NIH HHS/ -- R56 AI067544-01A1/AI/NIAID NIH HHS/ -- R56 AI067544-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006747" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD11b/immunology ; Astrocytes/immunology ; Central Nervous System Neoplasms/immunology ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Galectins/immunology ; Glioblastoma/immunology ; Humans ; Immunity, Innate ; Inflammation Mediators/*immunology ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Membrane Proteins/biosynthesis/*immunology ; Mice ; Microglia/immunology ; Multiple Sclerosis/immunology ; Rats ; Receptors, Immunologic/biosynthesis/*immunology ; Receptors, Virus/biosynthesis/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Th1 Cells/*immunology ; Toll-Like Receptors
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    Cancer. Converging on beta-catenin in Wilms tumor (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nusse, Roel -- New York, N.Y. -- Science. 2007 May 18;316(5827):988-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute, Stanford University, School of Medicine, Stanford, CA 94305-5323, USA. rnusse@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510350" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adenomatous Polyposis Coli Protein/metabolism ; Axin Protein ; Cell Nucleus/metabolism ; Chromosomes, Human, X/genetics ; Cytoplasm/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; *Genes, Wilms Tumor ; Humans ; Kidney Neoplasms/*genetics/metabolism ; Male ; Mutation ; Repressor Proteins/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/*genetics/*metabolism ; Wilms Tumor/*genetics/metabolism ; Wnt Proteins/metabolism ; beta Catenin/genetics/*metabolism
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    LRP6 mutation in a family with early coronary disease and metabolic risk factors (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: Coronary artery disease (CAD) is the leading cause of death worldwide and is commonly caused by a constellation of risk factors called the metabolic syndrome. We characterized a family with autosomal dominant early CAD, features of the metabolic syndrome (hyperlipidemia, hypertension, and diabetes), and osteoporosis. These traits showed genetic linkage to a short segment of chromosome 12p, in which we identified a missense mutation in LRP6, which encodes a co-receptor in the Wnt signaling pathway. The mutation, which substitutes cysteine for arginine at a highly conserved residue of an epidermal growth factor-like domain, impairs Wnt signaling in vitro. These results link a single gene defect in Wnt signaling to CAD and multiple cardiovascular risk factors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945222/" 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/PMC2945222/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, Arya -- Radhakrishnan, Jayaram -- Wang, He -- Mani, Alaleh -- Mani, Mohammad-Ali -- Nelson-Williams, Carol -- Carew, Khary S -- Mane, Shrikant -- Najmabadi, Hossein -- Wu, Dan -- Lifton, Richard P -- K08 HD041481/HD/NICHD NIH HHS/ -- K08 HD041481-01/HD/NICHD NIH HHS/ -- P01DK68229/DK/NIDDK NIH HHS/ -- P50 HL55007/HL/NHLBI NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 AR051476-04/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1278-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Howard Hughes Medical Institute and Yale University School of Medicine, New Haven, CT 06510, USA. arya.mani@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332414" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Amino Acid Substitution ; Animals ; Chromosomes, Human, Pair 12/genetics ; Coronary Disease/*genetics/metabolism ; Family Health ; Female ; Genetic Linkage ; *Genetic Predisposition to Disease ; Humans ; LDL-Receptor Related Proteins/*genetics/physiology ; Lipids/blood ; Low Density Lipoprotein Receptor-Related Protein-6 ; Male ; Metabolic Syndrome X/*genetics/metabolism ; Mice ; Middle Aged ; *Mutation, Missense ; NIH 3T3 Cells ; Osteoporosis/genetics ; Pedigree ; Risk Factors ; Signal Transduction ; Wnt Proteins/metabolism
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    Patterning mechanisms of branched organs (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Branching morphogenesis is one of the earliest events essential for the success of metazoans. By branching out and forming cellular or tissue extensions, cells can maximize their surface area and overcome space constraints posed by organ size. Over the past decade, tremendous progress has been made toward understanding the branching mechanisms of various invertebrate and vertebrate organ systems. Despite their distinct origins, morphologies and functions, different cell and tissue types use a remarkably conserved set of tools to undergo branching morphogenesis. Recent studies have shed important light on the basis of molecular conservation in the formation of branched structures in diverse organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645229/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Pengfei -- Werb, Zena -- CA057621/CA/NCI NIH HHS/ -- ES012801/ES/NIEHS NIH HHS/ -- R01 CA057621/CA/NCI NIH HHS/ -- R01 CA057621-16A1/CA/NCI NIH HHS/ -- U01 ES012801-06/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1506-9. doi: 10.1126/science.1162783.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Program in Developmental Biology, University of California at San Francisco, San Francisco, CA 94143-0452, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/embryology/physiology ; *Body Patterning ; Cell Differentiation ; Epithelium/embryology/physiology ; Genes ; Mesoderm/embryology/physiology ; *Morphogenesis ; Nervous System/embryology ; Neurons/cytology ; *Organogenesis ; Regeneration ; Signal Transduction ; Stem Cells/physiology ; Stromal Cells/physiology
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    Comment on "Genetically determined differences in learning from errors" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-16
    Description: Klein et al. (Reports, 7 December 2007, p. 1642) used individuals with a polymorphism adjacent to the dopamine receptor 2 gene as naturally occurring models for reduced brain dopamine receptor density in a probabilistic learning task. We raise the concern that this polymorphism resides in the gene for the kinase ANKK1, where it causes a nonconservative amino acid exchange.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lucht, Michael -- Rosskopf, Dieter -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):200; author reply 200. doi: 10.1126/science.1155372.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital for Psychiatry and Psychotherapy, Haus 30, Ernst-Moritz-Arndt University, Greifswald, Stralsund 18437, Germany. lucht@uni-greifswald.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18621654" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Brain/metabolism ; Cloning, Molecular ; Humans ; *Learning ; *Polymorphism, Genetic ; Protein-Serine-Threonine Kinases/*genetics/physiology ; Proteins/genetics/physiology ; Receptors, Dopamine D2/*genetics/metabolism ; Signal Transduction
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    Systems biology. Enlightening Rhythms (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipan, Ovidiu -- New York, N.Y. -- Science. 2008 Jan 25;319(5862):417-8. doi: 10.1126/science.1154208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of Richmond, Richmond, VA 23173, USA. olipan@richmond.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18218882" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; *Feedback, Physiological ; Gene Regulatory Networks ; Glycerol/*metabolism ; Mitogen-Activated Protein Kinases/genetics/metabolism ; *Models, Biological ; Osmolar Concentration ; Osmotic Pressure ; Saccharomyces cerevisiae/genetics/metabolism/*physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Signal Transduction ; Systems Biology
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    Tight regulation of unstructured proteins: from transcript synthesis to protein degradation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Altered abundance of several intrinsically unstructured proteins (IUPs) has been associated with perturbed cellular signaling that may lead to pathological conditions such as cancer. Therefore, it is important to understand how cells precisely regulate the availability of IUPs. We observed that regulation of transcript clearance, proteolytic degradation, and translational rate contribute to controlling the abundance of IUPs, some of which are present in low amounts and for short periods of time. Abundant phosphorylation and low stochasticity in transcription and translation indicate that the availability of IUPs can be finely tuned. Fidelity in signaling may require that most IUPs be available in appropriate amounts and not present longer than needed.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803065/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803065/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gsponer, Jorg -- Futschik, Matthias E -- Teichmann, Sarah A -- Babu, M Madan -- G0600158/Medical Research Council/United Kingdom -- MC_U105161047/Medical Research Council/United Kingdom -- MC_U105185859/Medical Research Council/United Kingdom -- U.1051.04.027.00001.01 (85859)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1365-8. doi: 10.1126/science.1163581.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK. jgsponer@mrc-lmb.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039133" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Cycle ; Computational Biology ; Genes, Fungal ; Humans ; Phosphorylation ; Protein Biosynthesis ; Protein Conformation ; Protein Kinases/metabolism ; Proteome/chemistry ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Saccharomyces cerevisiae/chemistry/cytology/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/*chemistry/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/chemistry/metabolism ; Signal Transduction ; Transcription, Genetic
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    The premetazoan ancestry of cadherins (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-16
    Description: Cadherin-mediated cell adhesion and signaling is essential for metazoan development and yet is absent from all other multicellular organisms. We found cadherin genes at numbers similar to those observed in complex metazoans in one of the closest single-celled relatives of metazoans, the choanoflagellate Monosiga brevicollis. Because the evolution of metazoans from a single-celled ancestor required novel cell adhesion and signaling mechanisms, the discovery of diverse cadherins in choanoflagellates suggests that cadherins may have contributed to metazoan origins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abedin, Monika -- King, Nicole -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):946-8. doi: 10.1126/science.1151084.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology and Center for Integrative Genomics, University of California at Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276888" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Amino Acid Sequence ; Animals ; Base Sequence ; *Biological Evolution ; Cadherins/*chemistry/*genetics/physiology ; Cell Adhesion ; Ciona intestinalis/chemistry ; Cnidaria/chemistry ; Drosophila melanogaster/chemistry ; Eukaryota/*chemistry ; Eukaryotic Cells/*chemistry/physiology ; Mice ; Molecular Sequence Data ; Protein Structure, Tertiary ; Repetitive Sequences, Amino Acid ; Signal Transduction ; Tyrosine/metabolism ; src Homology Domains
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    A genetic framework for the control of cell division and differentiation in the root meristem (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Plant growth and development are sustained by meristems. Meristem activity is controlled by auxin and cytokinin, two hormones whose interactions in determining a specific developmental output are still poorly understood. By means of a comprehensive genetic and molecular analysis in Arabidopsis, we show that a primary cytokinin-response transcription factor, ARR1, activates the gene SHY2/IAA3 (SHY2), a repressor of auxin signaling that negatively regulates the PIN auxin transport facilitator genes: thereby, cytokinin causes auxin redistribution, prompting cell differentiation. Conversely, auxin mediates degradation of the SHY2 protein, sustaining PIN activities and cell division. Thus, the cell differentiation and division balance necessary for controlling root meristem size and root growth is the result of the interaction between cytokinin and auxin through a simple regulatory circuit converging on the SHY2 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dello Ioio, Raffaele -- Nakamura, Kinu -- Moubayidin, Laila -- Perilli, Serena -- Taniguchi, Masatoshi -- Morita, Miyo T -- Aoyama, Takashi -- Costantino, Paolo -- Sabatini, Sabrina -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1380-4. doi: 10.1126/science.1164147.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartimento di Genetica e Biologia Molecolare, Laboratorio di Genomica e Proteomica Funzionale dei Sistemi Modello (FGPL), Universita La Sapienza - Piazzale Aldo Moro 5, 00185 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039136" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*cytology/genetics/growth & development/metabolism ; Arabidopsis Proteins/*genetics/*metabolism ; Cell Differentiation ; Cell Division ; Cytokinins/genetics/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation, Plant ; Genes, Plant ; Indoleacetic Acids/*metabolism ; Membrane Transport Proteins/genetics/metabolism ; Meristem/*cytology/growth & development ; Nuclear Proteins/*genetics/metabolism ; Plant Roots/*cytology/growth & development ; Promoter Regions, Genetic ; Signal Transduction ; Transcription Factors/genetics/*metabolism
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    Neuroscience. Rules of plasticity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brecht, Michael -- Schmitz, Dietmar -- New York, N.Y. -- Science. 2008 Jan 4;319(5859):39-40. doi: 10.1126/science.1153231.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bernstein Center for Computational Neuroscience, Humboldt-University Berlin, 10115 Berlin, Germany. michael.brecht@bccn-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174422" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association Learning ; Calcium/metabolism ; Long-Term Potentiation ; Memory ; Mice ; *Neuronal Plasticity ; Neurons/physiology ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Signal Transduction ; Somatosensory Cortex/cytology/*physiology ; Synapses/*physiology ; Synaptic Membranes/metabolism ; Vibrissae/innervation/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hepatic glucose sensing via the CREB coactivator CRTC2 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: Chronic hyperglycemia contributes to the development of diabetes-associated complications. Increases in the concentration of circulating glucose activate the hexosamine biosynthetic pathway (HBP) and promote the O-glycosylation of proteins by O-glycosyl transferase (OGT). We show that OGT triggered hepatic gluconeogenesis through the O-glycosylation of the transducer of regulated cyclic adenosine monophosphate response element-binding protein (CREB) 2 (TORC2 or CRTC2). CRTC2 was O-glycosylated at sites that normally sequester CRTC2 in the cytoplasm through a phosphorylation-dependent mechanism. Decreasing amounts of O-glycosylated CRTC2 by expression of the deglycosylating enzyme O-GlcNAcase blocked effects of glucose on gluconeogenesis, demonstrating the importance of the HBP in the development of glucose intolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dentin, Renaud -- Hedrick, Susan -- Xie, Jianxin -- Yates, John 3rd -- Montminy, Marc -- R01 GM037828/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1402-5. doi: 10.1126/science.1151363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323454" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Diabetes Mellitus/metabolism ; *Gluconeogenesis ; Glucose/*metabolism ; Glycosylation ; Glycosyltransferases/metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; RNA Interference ; Signal Transduction ; Trans-Activators/genetics/*metabolism ; Transcription Factors ; beta-N-Acetylhexosaminidases/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An agonist of toll-like receptor 5 has radioprotective activity in mouse and primate models (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: The toxicity of ionizing radiation is associated with massive apoptosis in radiosensitive organs. Here, we investigate whether a drug that activates a signaling mechanism used by tumor cells to suppress apoptosis can protect healthy cells from the harmful effects of radiation. We studied CBLB502, a polypeptide drug derived from Salmonella flagellin that binds to Toll-like receptor 5 (TLR5) and activates nuclear factor-kappaB signaling. A single injection of CBLB502 before lethal total-body irradiation protected mice from both gastrointestinal and hematopoietic acute radiation syndromes and resulted in improved survival. CBLB502 injected after irradiation also enhanced survival, but at lower radiation doses. It is noteworthy that the drug did not decrease tumor radiosensitivity in mouse models. CBLB502 also showed radioprotective activity in lethally irradiated rhesus monkeys. Thus, TLR5 agonists could potentially improve the therapeutic index of cancer radiotherapy and serve as biological protectants in radiation emergencies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322935/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burdelya, Lyudmila G -- Krivokrysenko, Vadim I -- Tallant, Thomas C -- Strom, Evguenia -- Gleiberman, Anatoly S -- Gupta, Damodar -- Kurnasov, Oleg V -- Fort, Farrel L -- Osterman, Andrei L -- Didonato, Joseph A -- Feinstein, Elena -- Gudkov, Andrei V -- AI066497/AI/NIAID NIH HHS/ -- CA75179/CA/NCI NIH HHS/ -- CA84406/CA/NCI NIH HHS/ -- R01 CA084406/CA/NCI NIH HHS/ -- R01 CA084406-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):226-30. doi: 10.1126/science.1154986.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403709" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/drug effects/radiation effects ; Chemotherapy, Adjuvant ; Flagellin/chemistry/pharmacology ; Gamma Rays ; Hematopoietic System/drug effects/radiation effects ; Intestine, Small/cytology/drug effects/radiation effects ; Macaca mulatta ; Mice ; Mice, Inbred ICR ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Neoplasms, Experimental/drug therapy/radiotherapy ; Peptides/administration & dosage/chemistry/*pharmacology/toxicity ; Radiation Dosage ; Radiation Injuries, Experimental/*prevention & control ; Radiation Tolerance/*drug effects ; Radiation-Protective Agents/administration & ; dosage/chemistry/*pharmacology/toxicity ; Salmonella enterica ; Signal Transduction ; Toll-Like Receptor 5/*agonists/metabolism ; Whole-Body Irradiation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A model for neuronal competition during development (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its own receptor TrkA in mouse and rat neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain-derived neurotrophic factor and neurotrophin-4, which, through the receptor p75, can kill neighboring neurons with low retrograde NGF-TrkA signaling whereas neurons with high NGF-TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deppmann, Christopher D -- Mihalas, Stefan -- Sharma, Nikhil -- Lonze, Bonnie E -- Niebur, Ernst -- Ginty, David D -- EY016281/EY/NEI NIH HHS/ -- F32 NS053187/NS/NINDS NIH HHS/ -- NS053187/NS/NINDS NIH HHS/ -- NS34814/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):369-73. doi: 10.1126/science.1152677. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Apoptosis ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Survival ; Cells, Cultured ; Computer Simulation ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Mathematics ; Mice ; *Models, Neurological ; Nerve Growth Factor/*metabolism ; Nerve Growth Factors/metabolism ; Neurons/cytology/*physiology ; Oligonucleotide Array Sequence Analysis ; Rats ; Receptor, trkA/genetics/*metabolism ; Receptors, Nerve Growth Factor/genetics/metabolism ; Signal Transduction ; Superior Cervical Ganglion/*cytology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Beta-catenin defines head versus tail identity during planarian regeneration and homeostasis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007
    Description: After amputation, freshwater planarians properly regenerate a head or tail from the resulting anterior or posterior wound. The mechanisms that differentiate anterior from posterior and direct the replacement of the appropriate missing body parts are unknown. We found that in the planarian Schmidtea mediterranea, RNA interference (RNAi) of beta-catenin or dishevelled causes the inappropriate regeneration of a head instead of a tail at posterior amputations. Conversely, RNAi of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration of a tail at anterior wounds. In addition, the silencing of beta-catenin is sufficient to transform the tail of uncut adult animals into a head. We suggest that beta-catenin functions as a molecular switch to specify and maintain anteroposterior identity during regeneration and homeostasis in planarians.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755502/" 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/PMC2755502/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurley, Kyle A -- Rink, Jochen C -- Sanchez Alvarado, Alejandro -- F32GM082016/GM/NIGMS NIH HHS/ -- R0-1 GM57260/GM/NIGMS NIH HHS/ -- R01 GM057260/GM/NIGMS NIH HHS/ -- R01 GM057260-08/GM/NIGMS NIH HHS/ -- T32CA093247/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):323-7. Epub 2007 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, Howard Hughes Medical Institute, University of Utah School of Medicine, 401 MREB, 20N 1900E, Salt Lake City, UT 84132, USA. sanchez@neuro.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063757" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/genetics/physiology ; Adenomatous Polyposis Coli Protein/chemistry/physiology ; Amino Acid Sequence ; Animals ; Body Patterning ; Gene Expression Profiling ; Genes, APC ; Head ; Helminth Proteins/chemistry/genetics/physiology ; Homeostasis ; Molecular Sequence Data ; Phosphoproteins/chemistry/genetics/physiology ; Planarians/genetics/*physiology ; RNA Interference ; *Regeneration ; Signal Transduction ; Tail ; beta Catenin/chemistry/genetics/*physiology
    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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    Comment on "Brain IRS2 signaling coordinates life span and nutrient homeostasis" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: Taguchi et al. (Reports, 20 July 2007, p. 369) reported that mice heterozygous for a null mutation in insulin receptor substrate-2 (Irs2) display a 17% increase in median life span. However, using the same mouse model, we find no evidence for life-span extension and suggest that the findings of Taguchi et al. were due to atypical life-span profiles in their study animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selman, Colin -- Lingard, Steven -- Gems, David -- Partridge, Linda -- Withers, Dominic J -- New York, N.Y. -- Science. 2008 May 23;320(5879):1012; author reply 1012. doi: 10.1126/science.1152366.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Diabetes and Endocrinology, Department of Medicine, University College London, Rayne Institute, 5 University Street, London WC1E 6JJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Crosses, Genetic ; Diet ; Female ; Homeostasis ; Insulin Receptor Substrate Proteins ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Kaplan-Meier Estimate ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phosphoproteins/genetics/*metabolism ; Research Design ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An integrated genomic analysis of human glioblastoma multiforme (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. To identify the genetic alterations in GBMs, we sequenced 20,661 protein coding genes, determined the presence of amplifications and deletions using high-density oligonucleotide arrays, and performed gene expression analyses using next-generation sequencing technologies in 22 human tumor samples. This comprehensive analysis led to the discovery of a variety of genes that were not known to be altered in GBMs. Most notably, we found recurrent mutations in the active site of isocitrate dehydrogenase 1 (IDH1) in 12% of GBM patients. Mutations in IDH1 occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival. These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Jones, Sian -- Zhang, Xiaosong -- Lin, Jimmy Cheng-Ho -- Leary, Rebecca J -- Angenendt, Philipp -- Mankoo, Parminder -- Carter, Hannah -- Siu, I-Mei -- Gallia, Gary L -- Olivi, Alessandro -- McLendon, Roger -- Rasheed, B Ahmed -- Keir, Stephen -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Busam, Dana A -- Tekleab, Hanna -- Diaz, Luis A Jr -- Hartigan, James -- Smith, Doug R -- Strausberg, Robert L -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Yan, Hai -- Riggins, Gregory J -- Bigner, Darell D -- Karchin, Rachel -- Papadopoulos, Nick -- Parmigiani, Giovanni -- Vogelstein, Bert -- Velculescu, Victor E -- Kinzler, Kenneth W -- 5P50-NS-20023/NS/NINDS NIH HHS/ -- CA09547/CA/NCI NIH HHS/ -- CA108786/CA/NCI NIH HHS/ -- CA11898/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- NS052507/NS/NINDS NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-160017/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R01 CA140316/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-27/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-13/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1807-12. doi: 10.1126/science.1164382. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics, and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772396" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/*genetics/mortality ; Female ; Gene Amplification ; Gene Dosage ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genome, Human ; Glioblastoma/*genetics/mortality ; Humans ; Isocitrate Dehydrogenase/chemistry/*genetics ; Male ; Middle Aged ; *Mutation ; Mutation, Missense ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Signal Transduction ; Survival Rate
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    Pyogenic bacterial infections in humans with MyD88 deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bernuth, Horst -- Picard, Capucine -- Jin, Zhongbo -- Pankla, Rungnapa -- Xiao, Hui -- Ku, Cheng-Lung -- Chrabieh, Maya -- Mustapha, Imen Ben -- Ghandil, Pegah -- Camcioglu, Yildiz -- Vasconcelos, Julia -- Sirvent, Nicolas -- Guedes, Margarida -- Vitor, Artur Bonito -- Herrero-Mata, Maria Jose -- Arostegui, Juan Ignacio -- Rodrigo, Carlos -- Alsina, Laia -- Ruiz-Ortiz, Estibaliz -- Juan, Manel -- Fortuny, Claudia -- Yague, Jordi -- Anton, Jordi -- Pascal, Mariona -- Chang, Huey-Hsuan -- Janniere, Lucile -- Rose, Yoann -- Garty, Ben-Zion -- Chapel, Helen -- Issekutz, Andrew -- Marodi, Laszlo -- Rodriguez-Gallego, Carlos -- Banchereau, Jacques -- Abel, Laurent -- Li, Xiaoxia -- Chaussabel, Damien -- Puel, Anne -- Casanova, Jean-Laurent -- U19 AI057234/AI/NIAID NIH HHS/ -- U19 AI057234-02/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):691-6. doi: 10.1126/science.1158298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, INSERM U550, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669862" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Bacterial Infections/*genetics/*immunology ; Cell Line, Transformed ; Child ; Child, Preschool ; Cytokines/metabolism ; Disease Susceptibility ; Female ; Gene Deletion ; Humans ; Immunity, Innate ; Male ; Mice ; Mutation, Missense ; Myeloid Differentiation Factor 88/*deficiency/genetics/metabolism ; Pneumococcal Infections/genetics/immunology ; Pseudomonas Infections/genetics/immunology ; Receptors, Interleukin-1/immunology/metabolism ; Signal Transduction ; Staphylococcal Infections/genetics/immunology ; Toll-Like Receptors/immunology/metabolism ; Transfection
    Print ISSN: 0036-8075
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    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
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    The serine protease TMPRSS6 is required to sense iron deficiency (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-05-03
    Description: Hepcidin, a liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron content. Several proteins induce expression of the hepcidin-encoding gene Hamp in response to infection or high levels of iron. However, mechanism(s) of Hamp suppression during iron depletion are poorly understood. We describe mask: a recessive, chemically induced mutant mouse phenotype, characterized by progressive loss of body (but not facial) hair and microcytic anemia. The mask phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is due to a splicing defect in the transmembrane serine protease 6 gene Tmprss6. Overexpression of normal TMPRSS6 protein suppresses activation of the Hamp promoter, and the TMPRSS6 cytoplasmic domain mediates Hamp suppression via proximal promoter element(s). TMPRSS6 is an essential component of a pathway that detects iron deficiency and blocks Hamp transcription, permitting enhanced dietary iron absorption.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430097/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Xin -- She, Ellen -- Gelbart, Terri -- Truksa, Jaroslav -- Lee, Pauline -- Xia, Yu -- Khovananth, Kevin -- Mudd, Suzanne -- Mann, Navjiwan -- Moresco, Eva Marie Y -- Beutler, Ernest -- Beutler, Bruce -- AI054523/AI/NIAID NIH HHS/ -- DK53505-09/DK/NIDDK NIH HHS/ -- R01 DK053505-09/DK/NIDDK NIH HHS/ -- U54 AI054523/AI/NIAID NIH HHS/ -- U54 AI054523-019005/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1088-92. doi: 10.1126/science.1157121. Epub 2008 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451267" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Macrocytic/genetics/metabolism ; Animals ; Antimicrobial Cationic Peptides/*genetics/metabolism ; Cell Line, Tumor ; Gene Expression Regulation ; Hepcidins ; Humans ; Iron/blood/*deficiency/metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Biological ; Mutation ; Phenotype ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Serine Endopeptidases/chemistry/genetics/*metabolism ; Signal Transduction ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Dichotomous dopaminergic control of striatal synaptic plasticity (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-08-09
    Description: At synapses between cortical pyramidal neurons and principal striatal medium spiny neurons (MSNs), postsynaptic D1 and D2 dopamine (DA) receptors are postulated to be necessary for the induction of long-term potentiation and depression, respectively-forms of plasticity thought to underlie associative learning. Because these receptors are restricted to two distinct MSN populations, this postulate demands that synaptic plasticity be unidirectional in each cell type. Using brain slices from DA receptor transgenic mice, we show that this is not the case. Rather, DA plays complementary roles in these two types of MSN to ensure that synaptic plasticity is bidirectional and Hebbian. In models of Parkinson's disease, this system is thrown out of balance, leading to unidirectional changes in plasticity that could underlie network pathology and symptoms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833421/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833421/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Weixing -- Flajolet, Marc -- Greengard, Paul -- Surmeier, D James -- DA10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- NS 34696/NS/NINDS NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-05/MH/NIMH NIH HHS/ -- R01 NS034696/NS/NINDS NIH HHS/ -- R01 NS034696-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 8;321(5890):848-51. doi: 10.1126/science.1160575.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18687967" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cannabinoid Receptor Modulators/metabolism ; Corpus Striatum/cytology/*physiology ; Dopamine/*physiology ; Glutamic Acid/metabolism ; *Long-Term Potentiation ; *Long-Term Synaptic Depression ; Mice ; Mice, Transgenic ; Neurons/*physiology ; Parkinsonian Disorders/*physiopathology ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; Signal Transduction ; Synapses/*physiology
    Print ISSN: 0036-8075
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    Inhibition of Rac by the GAP activity of centralspindlin is essential for cytokinesis (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-06
    Description: During cytokinesis, the guanosine triphosphatase (GTPase) RhoA orchestrates contractile ring assembly and constriction. RhoA signaling is controlled by the central spindle, a set of microtubule bundles that forms between the separating chromosomes. Centralspindlin, a protein complex consisting of the kinesin-6 ZEN-4 and the Rho family GTPase activating protein (GAP) CYK-4, is required for central spindle assembly and cytokinesis in Caenorhabditis elegans. However, the importance of the CYK-4 GAP activity and whether it regulates RhoA remain unclear. We found that two separation-of-function mutations in the GAP domain of CYK-4 lead to cytokinesis defects that mimic centralspindlin loss of function. These defects could be rescued by depletion of the GTPase Rac or its effectors, but not by depletion of RhoA. Thus, inactivation of Rac by centralspindlin functions in parallel with RhoA activation to drive contractile ring constriction during cytokinesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736296/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736296/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canman, Julie C -- Lewellyn, Lindsay -- Laband, Kimberley -- Smerdon, Stephen J -- Desai, Arshad -- Bowerman, Bruce -- Oegema, Karen -- GM058017/GM/NIGMS NIH HHS/ -- MC_U117584228/Medical Research Council/United Kingdom -- R01 GM049869/GM/NIGMS NIH HHS/ -- R01 GM049869-15/GM/NIGMS NIH HHS/ -- R01 GM058017/GM/NIGMS NIH HHS/ -- T32 CA067754/CA/NCI NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1543-6. doi: 10.1126/science.1163086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Biology, University of Oregon, Eugene, OR 97403, USA. jcanman@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056985" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Caenorhabditis elegans/*cytology/embryology/genetics/*metabolism ; Caenorhabditis elegans Proteins/*antagonists & ; inhibitors/chemistry/genetics/*metabolism ; *Cytokinesis ; Embryo, Nonmammalian/cytology/metabolism ; GTPase-Activating Proteins/chemistry/genetics/metabolism ; Genes, Helminth ; Kinesin/metabolism ; Mutation ; Protein Structure, Tertiary ; Signal Transduction ; Spindle Apparatus/physiology/ultrastructure ; rac GTP-Binding Proteins/*antagonists & inhibitors/metabolism ; rhoA GTP-Binding Protein/metabolism
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    Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-29
    Description: Schizophrenia is a devastating neurodevelopmental disorder whose genetic influences remain elusive. We hypothesize that individually rare structural variants contribute to the illness. Microdeletions and microduplications 〉100 kilobases were identified by microarray comparative genomic hybridization of genomic DNA from 150 individuals with schizophrenia and 268 ancestry-matched controls. All variants were validated by high-resolution platforms. Novel deletions and duplications of genes were present in 5% of controls versus 15% of cases and 20% of young-onset cases, both highly significant differences. The association was independently replicated in patients with childhood-onset schizophrenia as compared with their parents. Mutations in cases disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways. These results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, Tom -- McClellan, Jon M -- McCarthy, Shane E -- Addington, Anjene M -- Pierce, Sarah B -- Cooper, Greg M -- Nord, Alex S -- Kusenda, Mary -- Malhotra, Dheeraj -- Bhandari, Abhishek -- Stray, Sunday M -- Rippey, Caitlin F -- Roccanova, Patricia -- Makarov, Vlad -- Lakshmi, B -- Findling, Robert L -- Sikich, Linmarie -- Stromberg, Thomas -- Merriman, Barry -- Gogtay, Nitin -- Butler, Philip -- Eckstrand, Kristen -- Noory, Laila -- Gochman, Peter -- Long, Robert -- Chen, Zugen -- Davis, Sean -- Baker, Carl -- Eichler, Evan E -- Meltzer, Paul S -- Nelson, Stanley F -- Singleton, Andrew B -- Lee, Ming K -- Rapoport, Judith L -- King, Mary-Claire -- Sebat, Jonathan -- HD043569/HD/NICHD NIH HHS/ -- M01 RR000046/RR/NCRR NIH HHS/ -- MH061355/MH/NIMH NIH HHS/ -- MH061464/MH/NIMH NIH HHS/ -- MH061528/MH/NIMH NIH HHS/ -- NS052108/NS/NINDS NIH HHS/ -- R01 HD043569/HD/NICHD NIH HHS/ -- RR000046/RR/NCRR NIH HHS/ -- RR025014/RR/NCRR NIH HHS/ -- U01 MH061355/MH/NIMH NIH HHS/ -- U01 MH061464/MH/NIMH NIH HHS/ -- U01 MH061528/MH/NIMH NIH HHS/ -- U24 NS052108/NS/NINDS NIH HHS/ -- UL1 RR025014/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):539-43. doi: 10.1126/science.1155174. Epub 2008 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369103" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age of Onset ; Amino Acid Sequence ; Brain/cytology/*growth & development/metabolism ; Case-Control Studies ; Child ; Excitatory Amino Acid Transporter 1/chemistry/genetics/physiology ; Female ; *Gene Deletion ; *Gene Duplication ; Genetic Predisposition to Disease ; Genome, Human ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neurons/cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Receptor, Epidermal Growth Factor/chemistry/genetics/physiology ; Receptor, ErbB-4 ; Schizophrenia/*genetics/physiopathology ; Signal Transduction
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    Identification of SLEEPLESS, a sleep-promoting factor (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-19
    Description: Sleep is an essential process conserved from flies to humans. The importance of sleep is underscored by its tight homeostatic control. Through a forward genetic screen, we identified a gene, sleepless, required for sleep in Drosophila. The sleepless gene encodes a brain-enriched, glycosylphosphatidylinositol-anchored protein. Loss of SLEEPLESS protein caused an extreme (〉80%) reduction in sleep; a moderate reduction in SLEEPLESS had minimal effects on baseline sleep but markedly reduced the amount of recovery sleep after sleep deprivation. Genetic and molecular analyses revealed that quiver, a mutation that impairs Shaker-dependent potassium current, is an allele of sleepless. Consistent with this finding, Shaker protein levels were reduced in sleepless mutants. We propose that SLEEPLESS is a signaling molecule that connects sleep drive to lowered membrane excitability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771549/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771549/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, Kyunghee -- Joiner, William J -- Wu, Mark N -- Yue, Zhifeng -- Smith, Corinne J -- Sehgal, Amita -- AG017628/AG/NIA NIH HHS/ -- P01 AG017628/AG/NIA NIH HHS/ -- P01 AG017628-070004/AG/NIA NIH HHS/ -- R01 NS072431/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):372-6. doi: 10.1126/science.1155942.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635795" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Behavior, Animal ; Brain/metabolism ; Cell Membrane/metabolism ; DNA Transposable Elements ; Drosophila Proteins/chemistry/*genetics/*physiology ; Drosophila melanogaster/genetics/*physiology ; Female ; *Genes, Insect ; Glycosylphosphatidylinositols ; Homeostasis ; Longevity ; Male ; Membrane Proteins/chemistry/*genetics/*physiology ; *Models, Animal ; Molecular Sequence Data ; Mutation ; Phenotype ; Shaker Superfamily of Potassium Channels/physiology ; Signal Transduction ; *Sleep/genetics/physiology ; Sleep Deprivation ; Transgenes
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    Developmental biology. Aging of the ovary linked to PTEN pathway (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):558-9. doi: 10.1126/science.319.5863.558b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239099" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Female ; Forkhead Transcription Factors/genetics/physiology ; Humans ; Mice ; Oocytes/*physiology ; Ovarian Follicle/*physiology ; Ovulation ; PTEN Phosphohydrolase/antagonists & inhibitors/genetics/*physiology ; Primary Ovarian Insufficiency/*physiopathology/therapy ; Signal Transduction
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    Beta-arrestin-mediated localization of smoothened to the primary cilium (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-05-24
    Description: beta-Arrestins have important roles in the regulation of seven-transmembrane receptors (7TMRs). Smoothened (Smo) is a 7TMR that mediates effects of Hedgehog on developmental processes and whose dysregulation may cause tumorigenesis. beta-Arrestins are required for endocytosis of Smo and signaling to Gli transcription factors. In mammalian cells, Smo-dependent signaling requires translocation to primary cilia. We demonstrated that beta-arrestins mediate the activity-dependent interaction of Smo and the kinesin motor protein Kif3A. This multimeric complex localized to primary cilia and was disrupted in cells transfected with beta-arrestin small interfering RNA. beta-Arrestin 1 or beta-arrestin 2 depletion prevented the localization of Smo to primary cilia and the Smo-dependent activation of Gli. These results suggest roles for beta-arrestins in mediating the intracellular transport of a 7TMR to its obligate subcellular location for signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587210/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovacs, Jeffrey J -- Whalen, Erin J -- Liu, Renshui -- Xiao, Kunhong -- Kim, Jihee -- Chen, Minyong -- Wang, Jiangbo -- Chen, Wei -- Lefkowitz, Robert J -- 5R01 CA113656-02/CA/NCI NIH HHS/ -- 5T32 AI007217-25/AI/NIAID NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- HL70631/HL/NHLBI NIH HHS/ -- R01 CA113656/CA/NCI NIH HHS/ -- R01 CA113656-02/CA/NCI NIH HHS/ -- R01 CA113656-03/CA/NCI NIH HHS/ -- R01 HL016037/HL/NHLBI NIH HHS/ -- R01 HL016037-35/HL/NHLBI NIH HHS/ -- R01 HL070631/HL/NHLBI NIH HHS/ -- R01 HL070631-04/HL/NHLBI NIH HHS/ -- T32 AI007217/AI/NIAID NIH HHS/ -- T32 AI007217-25/AI/NIAID NIH HHS/ -- T32 AI007217-26/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1777-81. doi: 10.1126/science.1157983. Epub 2008 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*metabolism ; Cilia/*metabolism ; Hedgehog Proteins/metabolism ; Kinesin/*metabolism ; Mice ; Microscopy, Confocal ; Molecular Motor Proteins/*metabolism ; NIH 3T3 Cells ; Protein Transport ; RNA Interference ; Receptors, G-Protein-Coupled/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transfection
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    Dual origin of tissue-specific progenitor cells in Drosophila tracheal remodeling (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: During Drosophila metamorphosis, most larval cells die. Pupal and adult tissues form from imaginal cells, tissue-specific progenitors allocated in embryogenesis that remain quiescent during embryonic and larval life. Clonal analysis and fate mapping of single, identified cells show that tracheal system remodeling at metamorphosis involves a classical imaginal cell population and a population of differentiated, functional larval tracheal cells that reenter the cell cycle and regain developmental potency. In late larvae, both populations are activated and proliferate, spread over and replace old branches, and diversify into various stalk and coiled tracheolar cells under control of fibroblast growth factor signaling. Thus, Drosophila pupal/adult tissue progenitors can arise both by early allocation of multipotent cells and late return of differentiated cells to a multipotent state, even within a single tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999966/" 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/PMC3999966/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weaver, Molly -- Krasnow, Mark A -- R01 GM047735/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1496-9. doi: 10.1126/science.1158712. Epub 2008 Jul 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Cell Shape ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/*cytology/embryology/genetics/*growth & development ; Fibroblast Growth Factors/genetics/metabolism ; Gene Expression Regulation, Developmental ; Genes, Insect ; Larva/cytology/growth & development ; *Metamorphosis, Biological ; Multipotent Stem Cells/*cytology/physiology ; Protein-Tyrosine Kinases/genetics/metabolism ; Pupa/cytology/growth & development ; Receptors, Fibroblast Growth Factor/genetics/metabolism ; Signal Transduction ; Trachea/cytology/embryology/growth & development
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immunology. The toll of cathepsin K deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krieg, Arthur M -- Lipford, Grayson B -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):576-7. doi: 10.1126/science.1154207.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Coley Pharmaceutical Group, 93 Worcester Street, Wellesley, MA 02481, USA. akrieg@coleypharma.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*immunology/metabolism ; Cathepsin K ; Cathepsins/antagonists & inhibitors/deficiency/*metabolism ; Cytokines/secretion ; DNA, Bacterial/metabolism ; DNA, Viral/metabolism ; Dendritic Cells/immunology ; Dinucleoside Phosphates/immunology/metabolism ; Endoplasmic Reticulum/metabolism ; Endosomes/metabolism ; Humans ; *Immunity, Innate ; Inflammation/*immunology/metabolism ; Lysosomes/metabolism ; Mice ; Protease Inhibitors/pharmacology ; Rats ; Signal Transduction ; Toll-Like Receptor 9/antagonists & inhibitors/*metabolism
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  • 89
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    Physiology. Burn fat, live longer (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, Ting -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):865-6. doi: 10.1126/science.1166150.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA. tgx@stowersinstitute.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988829" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/metabolism ; Cell Proliferation ; Forkhead Transcription Factors ; Genes, Helminth ; Germ Cells/cytology/*metabolism ; Intestines/cytology/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Lipase/genetics/metabolism ; *Lipid Metabolism ; *Longevity ; Models, Animal ; Models, Biological ; Reproduction ; Signal Transduction ; Stem Cells/cytology/*metabolism ; Transcription Factors/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Dynamic analyses of Drosophila gastrulation provide insights into collective cell migration (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: The concerted movement of cells from different germ layers contributes to morphogenesis during early embryonic development. Using an optimized imaging approach and quantitative methods, we analyzed the trajectories of hundreds of ectodermal cells and internalized mesodermal cells within Drosophila embryos over 2 hours during gastrulation. We found a high level of cellular organization, with mesoderm cell movements correlating with some but not all ectoderm movements. During migration, the mesoderm population underwent two ordered waves of cell division and synchronous cell intercalation, and cells at the leading edge stably maintained position. Fibroblast growth factor (FGF) signaling guides mesodermal cell migration; however, we found some directed dorsal migration in an FGF receptor mutant, which suggests that additional signals are involved. Thus, decomposing complex cellular movements can provide detailed insights into collective cell migration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801059/" 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/PMC2801059/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMahon, Amy -- Supatto, Willy -- Fraser, Scott E -- Stathopoulos, Angelike -- P50 HG004071/HG/NHGRI NIH HHS/ -- R01 GM078542/GM/NIGMS NIH HHS/ -- R01 GM078542-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1546-50. doi: 10.1126/science.1167094.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; *Cell Movement ; Drosophila/*embryology/genetics/metabolism ; Ectoderm/*cytology ; Embryo, Nonmammalian/*cytology ; Fibroblast Growth Factors/metabolism ; *Gastrulation ; Mesoderm/*cytology ; Morphogenesis ; Mutation ; Phenotype ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    Ongoing in vivo experience triggers synaptic metaplasticity in the neocortex (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-01-05
    Description: In vivo experience can occlude subsequent induction of long-term potentiation and enhance long-term depression of synaptic responses. Although a reduced capacity for synaptic strengthening may function to prevent excessive excitation, such an effect paradoxically implies that continued experience or training should not improve and may even degrade neural representations. In mice, we examined the effect of ongoing whisker stimulation on synaptic strengthening at layer 4-2/3 synapses in the barrel cortex. Although N-methyl-d-aspartate receptors were required to initiate strengthening, they subsequently suppressed further potentiation at these synapses in vitro and in vivo. Despite this transition, synaptic strengthening continued with additional sensory activity but instead required the activation of metabotropic glutamate receptors, suggesting a mechanism by which continued experience can result in increasing synaptic strength over time.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clem, Roger L -- Celikel, Tansu -- Barth, Alison L -- DA017188-01/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2008 Jan 4;319(5859):101-4. doi: 10.1126/science.1143808.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association Learning ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Mice ; Mice, Transgenic ; Neocortex/*physiology ; *Neuronal Plasticity ; Neurons/physiology ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/chemistry ; Signal Transduction ; Somatosensory Cortex/*physiology ; Synapses/*physiology ; Vibrissae/*innervation/physiology
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  • 92
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    Phosphorylation networks regulating JNK activity in diverse genetic backgrounds (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-10-18
    Description: Cellular signaling networks have evolved to enable swift and accurate responses, even in the face of genetic or environmental perturbation. Thus, genetic screens may not identify all the genes that regulate different biological processes. Moreover, although classical screening approaches have succeeded in providing parts lists of the essential components of signaling networks, they typically do not provide much insight into the hierarchical and functional relations that exist among these components. We describe a high-throughput screen in which we used RNA interference to systematically inhibit two genes simultaneously in 17,724 combinations to identify regulators of Drosophila JUN NH(2)-terminal kinase (JNK). Using both genetic and phosphoproteomics data, we then implemented an integrative network algorithm to construct a JNK phosphorylation network, which provides structural and mechanistic insights into the systems architecture of JNK signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581798/" 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/PMC2581798/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakal, Chris -- Linding, Rune -- Llense, Flora -- Heffern, Elleard -- Martin-Blanco, Enrique -- Pawson, Tony -- Perrimon, Norbert -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):453-6. doi: 10.1126/science.1158739.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02215, USA. cbakal@receptor.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927396" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Line ; Computational Biology ; Drosophila/*enzymology/genetics ; Drosophila Proteins/genetics/*metabolism ; Fluorescence Resonance Energy Transfer ; *Genes, Insect ; JNK Mitogen-Activated Protein Kinases/genetics/*metabolism ; *MAP Kinase Signaling System ; Metabolic Networks and Pathways ; Phosphorylation ; Proteomics ; RNA Interference ; Signal Transduction
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    Developmental biology. Brain Wnts for blood vessels (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lammert, Eckhard -- New York, N.Y. -- Science. 2008 Nov 21;322(5905):1195-6. doi: 10.1126/science.1167451.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Animal Physiology, Heinrich-Heine-University, D-40225 Dusseldorf, Germany. lammert@uni-duesseldorf.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19023070" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Brain Barrier/embryology ; Brain/*blood supply/*embryology ; Embryonic Induction ; Humans ; Mice ; Neovascularization, Physiologic ; Signal Transduction ; Wnt Proteins/*physiology
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  • 94
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    Four-jointed is a Golgi kinase that phosphorylates a subset of cadherin domains (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-19
    Description: The atypical cadherin Fat acts as a receptor for a signaling pathway that regulates growth, gene expression, and planar cell polarity. Genetic studies in Drosophila identified the four-jointed gene as a regulator of Fat signaling. We show that four-jointed encodes a protein kinase that phosphorylates serine or threonine residues within extracellular cadherin domains of Fat and its transmembrane ligand, Dachsous. Four-jointed functions in the Golgi and is the first molecularly defined kinase that phosphorylates protein domains destined to be extracellular. An acidic sequence motif (Asp-Asn-Glu) within Four-jointed was essential for its kinase activity in vitro and for its biological activity in vivo. Our results indicate that Four-jointed regulates Fat signaling by phosphorylating cadherin domains of Fat and Dachsous as they transit through the Golgi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562711/" 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/PMC2562711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishikawa, Hiroyuki O -- Takeuchi, Hideyuki -- Haltiwanger, Robert S -- Irvine, Kenneth D -- CA123071/CA/NCI NIH HHS/ -- GM061126/GM/NIGMS NIH HHS/ -- GM078620/GM/NIGMS NIH HHS/ -- R01 CA123071/CA/NCI NIH HHS/ -- R01 CA123071-02/CA/NCI NIH HHS/ -- R01 GM061126/GM/NIGMS NIH HHS/ -- R01 GM061126-08/GM/NIGMS NIH HHS/ -- R01 GM078620/GM/NIGMS NIH HHS/ -- R01 GM078620-02/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):401-4. doi: 10.1126/science.1158159.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635802" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cadherins/chemistry/*metabolism ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster ; Electrophoretic Mobility Shift Assay ; Glycosylation ; Golgi Apparatus/enzymology/*metabolism ; Kinetics ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Phosphorylation ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism
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  • 95
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    Membrane phosphatidylserine regulates surface charge and protein localization (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-01-12
    Description: Electrostatic interactions with negatively charged membranes contribute to the subcellular targeting of proteins with polybasic clusters or cationic domains. Although the anionic phospholipid phosphatidylserine is comparatively abundant, its contribution to the surface charge of individual cellular membranes is unknown, partly because of the lack of reagents to analyze its distribution in intact cells. We developed a biosensor to study the subcellular distribution of phosphatidylserine and found that it binds the cytosolic leaflets of the plasma membrane, as well as endosomes and lysosomes. The negative charge associated with the presence of phosphatidylserine directed proteins with moderately positive charge to the endocytic pathway. More strongly cationic proteins, normally associated with the plasma membrane, relocalized to endocytic compartments when the plasma membrane surface charge decreased on calcium influx.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Gilbert, Gary E -- Shi, Jialan -- Silvius, John -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):210-3. doi: 10.1126/science.1152066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hospital for Sick Children, Toronto M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biosensing Techniques ; Cell Line ; Cell Membrane/*metabolism ; Endocytosis ; Endosomes/*metabolism ; Fluorescence ; Fluorescence Resonance Energy Transfer ; Humans ; Hydrophobic and Hydrophilic Interactions ; Intracellular Membranes/*metabolism ; Lysosomes/*metabolism ; Microscopy, Confocal ; Milk Proteins/metabolism ; Organelles/metabolism ; Phosphatidylserines/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Signal Transduction ; Static Electricity ; Surface Properties
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    Generation and regeneration of cells of the liver and pancreas (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-06
    Description: Liver and pancreas progenitors develop from endoderm cells in the embryonic foregut. Shortly after their specification, liver and pancreas progenitors rapidly acquire markedly different cellular functions and regenerative capacities. These changes are elicited by inductive signals and genetic regulatory factors that are highly conserved among vertebrates. Interest in the development and regeneration of the organs has been fueled by the intense need for hepatocytes and pancreatic beta cells in the therapeutic treatment of liver failure and type I diabetes. Studies in diverse model organisms have revealed evolutionarily conserved inductive signals and transcription factor networks that elicit the differentiation of liver and pancreatic cells and provide guidance for how to promote hepatocyte and beta cell differentiation from diverse stem and progenitor cell types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2641009/" 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/PMC2641009/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaret, Kenneth S -- Grompe, Markus -- P30 CA006927/CA/NCI NIH HHS/ -- P30 CA006927-46/CA/NCI NIH HHS/ -- P30CA06927/CA/NCI NIH HHS/ -- R01 DK051592/DK/NIDDK NIH HHS/ -- R01 DK051592-11/DK/NIDDK NIH HHS/ -- R01 GM036477/GM/NIGMS NIH HHS/ -- R01 GM036477-21/GM/NIGMS NIH HHS/ -- R0I DK05192/DK/NIDDK NIH HHS/ -- R37 GM36477/GM/NIGMS NIH HHS/ -- U01 DK072477/DK/NIDDK NIH HHS/ -- U01 DK072477-04/DK/NIDDK NIH HHS/ -- U01 DK072503/DK/NIDDK NIH HHS/ -- U01 DK072503-04/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1490-4. doi: 10.1126/science.1161431.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Epigenetics and Progenitor Cells Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA. zaret@fccc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056973" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Transdifferentiation ; Endoderm/embryology ; Hepatocytes/*cytology ; Humans ; Insulin-Secreting Cells/*cytology ; Liver/cytology/*embryology/physiology ; Liver Regeneration ; Morphogenesis ; Organogenesis ; Pancreas/*cytology/*embryology/physiology ; *Regeneration ; Signal Transduction ; Stem Cells/*cytology/physiology ; Transcription Factors/genetics/metabolism
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    Cell biology. RNA metabolism and oncogenesis (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Deborah L -- Johnson, Sandra A S -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):461-2. doi: 10.1126/science.1158680.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, CA 90033, USA. johnsond@hsc.usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; *Cell Transformation, Neoplastic ; Mice ; Nuclear Proteins/metabolism ; *Protein Biosynthesis ; RNA/genetics/*metabolism ; RNA Polymerase III/*metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Ribosomal/metabolism ; RNA, Transfer/*metabolism ; RNA, Transfer, Met/metabolism ; RNA-Binding Proteins/metabolism ; Signal Transduction ; Transcription Factors, General/metabolism ; Transcription Factors, TFIII/metabolism ; *Transcription, Genetic
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    Reward-predictive cues enhance excitatory synaptic strength onto midbrain dopamine neurons (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: Using sensory information for the prediction of future events is essential for survival. Midbrain dopamine neurons are activated by environmental cues that predict rewards, but the cellular mechanisms that underlie this phenomenon remain elusive. We used in vivo voltammetry and in vitro patch-clamp electrophysiology to show that both dopamine release to reward predictive cues and enhanced synaptic strength onto dopamine neurons develop over the course of cue-reward learning. Increased synaptic strength was not observed after stable behavioral responding. Thus, enhanced synaptic strength onto dopamine neurons may act to facilitate the transformation of neutral environmental stimuli to salient reward-predictive cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613864/" 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/PMC2613864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stuber, Garret D -- Klanker, Marianne -- de Ridder, Bram -- Bowers, M Scott -- Joosten, Ruud N -- Feenstra, Matthijs G -- Bonci, Antonello -- DA015096/DA/NIDA NIH HHS/ -- DA021937/DA/NIDA NIH HHS/ -- R01 DA015096/DA/NIDA NIH HHS/ -- R01 DA015096-06/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1690-2. doi: 10.1126/science.1160873.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18802002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Cues ; Dopamine/*physiology ; Excitatory Postsynaptic Potentials ; *Learning ; Long-Term Potentiation ; Male ; Mesencephalon/cytology/*physiology ; Neurons/*physiology ; Nucleus Accumbens/*physiology ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; *Reward ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission
    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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  • 99
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    Segregation of axial motor and sensory pathways via heterotypic trans-axonal signaling (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: Execution of motor behaviors relies on circuitries effectively integrating immediate sensory feedback to efferent pathways controlling muscle activity. It remains unclear how, during neuromuscular circuit assembly, sensory and motor projections become incorporated into tightly coordinated, yet functionally separate pathways. We report that, within axial nerves, establishment of discrete afferent and efferent pathways depends on coordinate signaling between coextending sensory and motor projections. These heterotypic axon-axon interactions require motor axonal EphA3/EphA4 receptor tyrosine kinases activated by cognate sensory axonal ephrin-A ligands. Genetic elimination of trans-axonal ephrin-A --〉 EphA signaling in mice triggers drastic motor-sensory miswiring, culminating in functional efferents within proximal afferent pathways. Effective assembly of a key circuit underlying motor behaviors thus critically depends on trans-axonal signaling interactions resolving motor and sensory projections into discrete pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158657/" 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/PMC3158657/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallarda, Benjamin W -- Bonanomi, Dario -- Muller, Daniel -- Brown, Arthur -- Alaynick, William A -- Andrews, Shane E -- Lemke, Greg -- Pfaff, Samuel L -- Marquardt, Till -- NS031249-14A1/NS/NINDS NIH HHS/ -- NS054172-01A2/NS/NINDS NIH HHS/ -- R01 NS054172/NS/NINDS NIH HHS/ -- R01 NS054172-01A2/NS/NINDS NIH HHS/ -- R01 NS054172-02/NS/NINDS NIH HHS/ -- R01 NS054172-03/NS/NINDS NIH HHS/ -- R01 NS054172-04/NS/NINDS NIH HHS/ -- R01 NS054172-05/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):233-6. doi: 10.1126/science.1153758.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression 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/18403711" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/physiology ; Animals ; Axons/*physiology ; Cells, Cultured ; Coculture Techniques ; Efferent Pathways/physiology ; Electrophysiology ; Ephrins/*metabolism ; Ganglia, Spinal/cytology/physiology ; Growth Cones/physiology ; Ligands ; Mice ; Mice, Transgenic ; Motor Activity ; Motor Neurons/*physiology ; Muscle, Skeletal/innervation ; Mutation ; Neurons, Afferent/*physiology ; Peripheral Nerves/cytology/physiology ; Receptor, EphA3/genetics/*metabolism ; Receptor, EphA4/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 100
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    Cell biology. Arrestin' movement in cilia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohatgi, Rajat -- Scott, Matthew P -- 1K99CA129174/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1726-7. doi: 10.1126/science.1160448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305-5439, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18583599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*metabolism ; Cells, Cultured ; Cilia/*metabolism ; Hedgehog Proteins/metabolism ; Kinesin/*metabolism ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Molecular Motor Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Protein Transport ; RNA Interference ; Receptors, G-Protein-Coupled/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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