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Science 8 May 1992:
Vol. 256. no. 5058, pp. 825 - 827
DOI: 10.1126/science.1317056
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Articles

Science, Vol 256, Issue 5058, 825-827
Copyright © 1992 by American Association for the Advancement of Science

articles

Implication of GAP in Ras-dependent transactivation of a polyoma enhancer sequence

F Schweighoffer, I Barlat, MC Chevallier-Multon, and B Tocque

Rhone-Poulenc Rorer, Centre de Recherche de Vitry-Alfortville, Vitry Sur Seine.

Controversy exists as to whether the interaction of a guanosine triphosphatase activating protein (GAP) with Ras proteins functions both to initiate and to terminate Ras-dependent signaling events or only to terminate them. GAP-C, a carboxyl-terminal fragment of GAP that is sufficient to stimulate GTPase activity, inhibited the stimulation of transcription produced by some oncoproteins (v-Src, polyoma middle T, wild-type Ras, and oncogenic Ras) but not that produced by v-Mos. Wild-type GAP did not affect transcription induced by oncogenic Ras but reversed the inhibitory effect of GAP-C on transcription induced by oncogenic Ras. These results indicate that GAP is a negative regulator of wild-type Ras and elicits a downstream signal by interacting with Ras-GTP (guanosine triphosphate).


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