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  • Carbachol/pharmacology  (1)
  • American Association for the Advancement of Science (AAAS)  (1)
  • Mineralogical Society of Great Britain and Ireland
  • 1995-1999  (1)
  • 1980-1984
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  • American Association for the Advancement of Science (AAAS)  (1)
  • Mineralogical Society of Great Britain and Ireland
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  • 1995-1999  (1)
  • 1980-1984
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    Publikationsdatum: 1997-06-20
    Beschreibung: Various receptors coupled to the heterotrimeric guanine nucleotide-binding protein Gq/11 stimulate formation of inositol-1,4,5-trisphosphate (IP3). Activation of these receptors also induces protein tyrosine phosphorylation. Formation of IP3 in response to stimulated receptors that couple to Gq/11 was blocked by protein tyrosine kinase inhibitors. These inhibitors appeared to act before activation of Gq/11. Moreover, stimulation of receptors coupled to Gq/11 induced phosphorylation on a tyrosine residue (Tyr356) of the Galphaq/11 subunit, and this tyrosine phosphorylation event was essential for Gq/11 activation. Tyrosine phosphorylation of Galphaq/11 induced changes in its interaction with receptors. Therefore, tyrosine phosphorylation of Galphaq/11 appears to regulate the activation of Gq/11 protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umemori, H -- Inoue, T -- Kume, S -- Sekiyama, N -- Nagao, M -- Itoh, H -- Nakanishi, S -- Mikoshiba, K -- Yamamoto, T -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1878-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188537" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CHO Cells ; Calcium/metabolism ; Carbachol/pharmacology ; Cell Line ; Cricetinae ; Enzyme Inhibitors/pharmacology ; GTP-Binding Proteins/*metabolism ; Genistein ; Inositol 1,4,5-Trisphosphate/metabolism ; Isoflavones/pharmacology ; Phosphorylation ; Phosphotyrosine/*metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Receptors, Cholinergic/*metabolism ; Receptors, Metabotropic Glutamate/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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