Inhibition of GTPase activating protein stimulation of Ras-p21 GTPase by the Krev-1 gene product

被引：247

作者：

Frech, M

John, J

Pizon, V

Chardin, P

Tavitian, A

Clark, R

Mccormick, F

Wittinghofer, A ^{[1
]}

机构：

[1] Max Planck Inst Med Forsch, Abt Biophys, Jahnstr 29, D-6900 Heidelberg, GERMANY

[2] INSERM, U248, Fac Med Lariboisiere St Louis, F-75010 Paris, FRANCE

[3] Cetus Corp, Dept Mol Biol, Emeryville, CA 94608 USA

来源：

SCIENCE | 1990年 / 249卷 / 4965期

关键词：

D O I：

10.1126/science.2164710

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Krev-1 is known to suppress transformation by ras. However, the mechanism of the suppression is unclear. The protein product of Krev-1, Rap1A-p21, is identical to Rasp21 proteins in the region where interaction with guanosine triphosphatase (GTPase) activating protein (GAP) is believed to occur. Therefore, the ability of GAP to interact with Rap1A-p21 was tested. Rap1A-p21 was not activated by GAP but bound tightly to GAP and was an effective competitive inhibitor of GAP-mediated Ras-GTPase activity. Binding of GAP to Rap1A-p21 was strictly guanosine triphosphate (GTP)-dependent. The ability of Rap1A-p21 to bind tightly to GAP may account for Krev-1 suppression of transformation by ras. This may occur by preventing interaction of GAP with Ras-p21 or with other cellular proteins necessary for GAP-mediated Ras GTPase activity.

引用

页码：169 / 171

页数：3

共 24 条

[1] GUANOSINE TRIPHOSPHATASE ACTIVATING PROTEIN (GAP) INTERACTS WITH THE P21-RAS EFFECTOR BINDING DOMAIN [J].