| Author(s) | LUTTRELL LM; VANBIESEN T; HAWES BE; KOCH WJ; TOUHARA K; LEFKOWITZ RJ
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| Title | G(BETA-GAMMA) SUBUNITS MEDIATE MITOGEN-ACTIVATED PROTEIN-KINASE ACTIVATION BY THE TYROSINE KINASE INSULIN-LIKE GROWTH-FACTOR-1 RECEPTOR
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| Source | JOURNAL OF BIOLOGICAL CHEMISTRY 270 (28): 16495-16498
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| Date | 1995 JUL 14
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| Type | Journal : Note
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| LCR: 6 NCR: 41 LCS: 11 GCS: 131
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| Address | DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DURHAM,NC 27710.
DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710.
DUKE UNIV,MED CTR,DEPT BIOCHEM,DURHAM,NC 27710.
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| Abstract | The receptors for insulin-like growth factor 1 (IGF1) and insulin are related heterotetrameric proteins which, like the epidermal growth factor (EGF) receptor, possess intrinsic ligand-stimulated tyrosine protein kinase activity, In Rat 1 fibroblasts, stimulation of mitogen-activated protein (MAP) kinase via the IGF1 receptor and the G(i)- coupled receptor for lysophosphatidic acid (LPA), but not via the EGF receptor, is sensitive both to pertussis toxin treatment and to cellular expression of a specific G(beta gamma) subunit-binding peptide, The IGF1, LPA, and EGF receptor-mediated signals are all sensitive to inhibitors of tyrosine protein kinases, require p21(ras) activation, and are independent of protein kinase C. These data suggest that some tyrosine kinase growth factor receptors (e.g. IGF1 receptor) and classical G protein-coupled receptors (e.g. LPA receptor) employ a similar mechanism for mitogenic signaling that involves both tyrosine phosphorylation and G(beta gamma) subunits derived from pertussis toxin-sensitive G proteins.
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