RAS-GTPASE ACTIVATING PROTEIN (GAP) - A PUTATIVE EFFECTOR FOR RAS

Citation
B. Tocque et al., RAS-GTPASE ACTIVATING PROTEIN (GAP) - A PUTATIVE EFFECTOR FOR RAS, Cellular signalling, 9(2), 1997, pp. 153-158
Citations number
71
Categorie Soggetti
Biology,"Cell Biology
Journal title
ISSN journal
08986568
Volume
9
Issue
2
Year of publication
1997
Pages
153 - 158
Database
ISI
SICI code
0898-6568(1997)9:2<153:RAP(-A>2.0.ZU;2-B
Abstract
One attractive candidate for a Pas effector protein, other than the Ra f kinases, is Ras-GAP. Indeed, recent literature suggests that besides the Raf/MAP kinase cascade, additional pathways must be stimulated to elicit a full biological response to Ras. Ras binds the COOH terminal domain of Ras-GAP, while the NH2 terminal domain appears to be essent ial for triggering downstream signals. Since Ras-GAP itself has no obv ious enzymatic function that might explain a role in processes associa ted with proliferation, differentiation or apoptosis, candidates for d ownstream Ras GAP effecters that fulfill this role remain to be identi fied. The newly found GAP-SH3 domain Binding Protein (G3BP) may be one of these. This review will briefly overview the candidates Pas effect ers and discuss the results that position Ras-GAP as a critical effect or downstream of Ras. (C) 1997 Elsevier Science Inc.