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  • 1
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    Filopodial calcium transients promote substrate-dependent growth cone turning (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2001-03-10
    Beschreibung: Filopodia that extend from neuronal growth cones sample the environment for extracellular guidance cues, but the signals they transmit to growth cones are unknown. Filopodia were observed generating localized transient elevations of intracellular calcium ([Ca2+]i) that propagate back to the growth cone and stimulate global Ca2+ elevations. The frequency of filopodial Ca2+ transients was substrate-dependent and may be due in part to influx of Ca2+ through channels activated by integrin receptors. These transients slowed neurite outgrowth by reducing filopodial motility and promoted turning when stimulated differentially within filopodia on one side of the growth cone. These rapid signals appear to serve both as autonomous regulators of filopodial movement and as frequency-coded signals integrated within the growth cone and could be a common signaling process for many motile cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez, T M -- Robles, E -- Poo , M -- Spitzer, N C -- New York, N.Y. -- Science. 2001 Mar 9;291(5510):1983-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Center for Molecular Genetics, University of California, San Diego, La Jolla, CA 92093, USA. tmgomez@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11239161" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD29/metabolism ; Calcium/*metabolism ; *Calcium Signaling ; Cell Movement ; Cells, Cultured ; Culture Techniques ; Embryo, Nonmammalian/cytology ; Growth Cones/metabolism/*physiology ; Integrins/metabolism ; Laminin/pharmacology ; Microscopy, Confocal ; Neurites/metabolism/*physiology ; Neurons/physiology ; Oligopeptides/pharmacology ; Pseudopodia/*metabolism ; Tenascin/pharmacology ; Xenopus/embryology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    G-protein signaling through tubby proteins (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2001-05-26
    Beschreibung: Dysfunction of the tubby protein results in maturity-onset obesity in mice. Tubby has been implicated as a transcription regulator, but details of the molecular mechanism underlying its function remain unclear. Here we show that tubby functions in signal transduction from heterotrimeric GTP-binding protein (G protein)-coupled receptors. Tubby localizes to the plasma membrane by binding phosphatidylinositol 4,5-bisphosphate through its carboxyl terminal "tubby domain." X-ray crystallography reveals the atomic-level basis of this interaction and implicates tubby domains as phosphorylated-phosphatidyl- inositol binding factors. Receptor-mediated activation of G protein alphaq (Galphaq) releases tubby from the plasma membrane through the action of phospholipase C-beta, triggering translocation of tubby to the cell nucleus. The localization of tubby-like protein 3 (TULP3) is similarly regulated. These data suggest that tubby proteins function as membrane-bound transcription regulators that translocate to the nucleus in response to phosphoinositide hydrolysis, providing a direct link between G-protein signaling and the regulation of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santagata, S -- Boggon, T J -- Baird, C L -- Gomez, C A -- Zhao, J -- Shan, W S -- Myszka, D G -- Shapiro, L -- New York, N.Y. -- Science. 2001 Jun 15;292(5524):2041-50. Epub 2001 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ruttenberg Cancer Center, Structural Biology Program, Department of Physiology and Biophysics, Mount Sinai School of Medicine of New York University, 1425 Madison Avenue New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11375483" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus ; Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Cell Membrane/metabolism ; Cell Nucleus/*metabolism ; Cells, Cultured ; Crystallography, X-Ray ; GTP-Binding Protein alpha Subunits, Gq-G11 ; Gene Expression Regulation ; Heterotrimeric GTP-Binding Proteins/*metabolism ; Humans ; Isoenzymes/*metabolism ; Membrane Lipids/metabolism ; Mice ; Models, Biological ; Molecular Sequence Data ; Nuclear Localization Signals ; Obesity/genetics/metabolism ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C beta ; Phosphorylation ; Protein Structure, Tertiary ; Proteins/chemistry/genetics/*metabolism ; Receptor, Serotonin, 5-HT2C ; Receptors, Muscarinic/metabolism ; Receptors, Serotonin/metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transcription Factors/chemistry/genetics/*metabolism ; Type C Phospholipases/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Integrase inhibitors and cellular immunity suppress retroviral replication in rhesus macaques (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-07-13
    Beschreibung: We describe the efficacy of L-870812, an inhibitor of HIV-1 and SIV integrase, in rhesus macaques infected with the simian-human immunodeficiency virus (SHIV) 89.6P. When initiated before CD4 cell depletion, L-870812 therapy mediated a sustained suppression of viremia, preserving CD4 levels and permitting the induction of virus-specific cellular immunity. L-870812 was also active in chronic infection; however, the magnitude and durability of the effect varied in conjunction with the pretreatment immune response and viral load. These studies demonstrate integrase inhibitor activity in vivo and suggest that cellular immunity facilitates chemotherapeutic efficacy in retroviral infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hazuda, Daria J -- Young, Steven D -- Guare, James P -- Anthony, Neville J -- Gomez, Robert P -- Wai, John S -- Vacca, Joseph P -- Handt, Larry -- Motzel, Sherri L -- Klein, Hilton J -- Dornadula, Geethanjali -- Danovich, Robert M -- Witmer, Marc V -- Wilson, Keith A A -- Tussey, Lynda -- Schleif, William A -- Gabryelski, Lori S -- Jin, Lixia -- Miller, Michael D -- Casimiro, Danilo R -- Emini, Emilio A -- Shiver, John W -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):528-32. Epub 2004 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Merck Research Laboratories, Post Office Box 4, West Point, PA 19486, USA. daria_hazuda@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247437" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acquired Immunodeficiency Syndrome/*drug therapy/*immunology/virology ; Animals ; Anti-HIV Agents/administration & dosage/blood/pharmacology/therapeutic use ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Drug Resistance, Viral ; HIV Integrase/genetics/metabolism ; HIV Integrase Inhibitors/administration & dosage/blood/pharmacology/therapeutic ; use ; HIV-1/drug effects/enzymology/genetics/*physiology ; Immunity, Cellular ; Integrase Inhibitors/administration & dosage/blood/pharmacology/*therapeutic use ; Integrases/genetics/metabolism ; Leukocytes, Mononuclear/virology ; Macaca mulatta ; Mutation ; Naphthyridines/administration & dosage/blood/pharmacology/*therapeutic use ; Simian Acquired Immunodeficiency Syndrome/*drug therapy/*immunology/virology ; Simian Immunodeficiency Virus/drug effects/enzymology/genetics/*physiology ; Viral Load ; Viremia/drug therapy ; Virus Replication/drug effects
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
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