endothelin-1 and Neuroectodermal-Tumors--Primitive--Peripheral

endothelin-1 has been researched along with Neuroectodermal-Tumors--Primitive--Peripheral* in 1 studies

Other Studies

1 other study(ies) available for endothelin-1 and Neuroectodermal-Tumors--Primitive--Peripheral

Article	Year
Potentiation of G-protein-coupled receptor-induced MAP kinase activation by exogenous EGF receptors in SK-N-MC neuroepithelioma cells. Biochemical and biophysical research communications, 1998, Oct-09, Volume: 251, Issue:1 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. Topics: Animals; Calcium; Calcium-Calmodulin-Dependent Protein Kinases; COS Cells; Drug Synergism; Endothelin-1; Enzyme Activation; ErbB Receptors; GTP-Binding Proteins; Humans; Lysophospholipids; Neuroectodermal Tumors, Primitive, Peripheral; Receptors, Cell Surface; Transcriptional Activation; Tumor Cells, Cultured	1998

Article

Year

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

Biochemical and biophysical research communications, 1998, Oct-09, Volume: 251, Issue:1

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.

Topics: Animals; Calcium; Calcium-Calmodulin-Dependent Protein Kinases; COS Cells; Drug Synergism; Endothelin-1; Enzyme Activation; ErbB Receptors; GTP-Binding Proteins; Humans; Lysophospholipids; Neuroectodermal Tumors, Primitive, Peripheral; Receptors, Cell Surface; Transcriptional Activation; Tumor Cells, Cultured

1998