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Potentiation of G-protein-coupled receptor-induced MAP kinase activation by exogenous EGF receptors in SK-N-MC neuroepithelioma cells.

Abstract
Lysophosphatidic acid (LPA) and endothelin-1 (ET-1), two ligands for G-protein coupled receptors (GPCRs), induce activation of mitogen activated protein kinase (MAPK). Surprisingly, LPA and ET-1 did not induce MAPK activation in SK-N-MC neuroepithelioma cells, even though these GPCR ligands evoked a rapid, transient rise in intracellular free Ca2+ concentration in these cells, indicating that SK-N-MC cells express functional LPA- and ET-1-receptors. Transient transfection of the EGFR into SK-N-MC cells, which do not express endogenous EGFR, potentiated LPA- and ET-1-induced MAPK activation. LPA and ET-1 did not enhance basal level tyrosine phosphorylation of the transfected EGFR in SK-N-MC cells. Even though the mechanism of LPA- and ET-1-induced MAPK activation in EGFR-transfected SK-N-MC cells remains to be determined definitively, our results provide strong evidence that the EGFR links these GPCRs to MAPK activation.
AuthorsA Buist, L G Tertoolen, J den Hertog
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 251 Issue 1 Pg. 6-10 (Oct 09 1998) ISSN: 0006-291X [Print] United States
PMID9790898 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright 1998 Academic Press.
Chemical References
  • Endothelin-1
  • Lysophospholipids
  • Receptors, Cell Surface
  • ErbB Receptors
  • Calcium-Calmodulin-Dependent Protein Kinases
  • GTP-Binding Proteins
  • Calcium
Topics
  • Animals
  • COS Cells
  • Calcium (metabolism)
  • Calcium-Calmodulin-Dependent Protein Kinases (metabolism)
  • Drug Synergism
  • Endothelin-1 (pharmacology)
  • Enzyme Activation (drug effects)
  • ErbB Receptors (biosynthesis, metabolism, physiology)
  • GTP-Binding Proteins (metabolism, physiology)
  • Humans
  • Lysophospholipids (metabolism)
  • Neuroectodermal Tumors, Primitive, Peripheral (metabolism)
  • Receptors, Cell Surface (physiology)
  • Transcriptional Activation
  • Tumor Cells, Cultured

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