Rac1 is required for cell proliferation and G2/M progression

被引：72
作者：
Moore, KA
Sethi, R
Doanes, AM
Johnson, TM
Pracyk, JB
Kirby, M
Irani, K
GoldschmidtClermont, PJ
Finkel, T
机构：
[1] NHLBI,CARDIOL BRANCH,NATL INST HLTH,BETHESDA,MD 20892
[2] NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892
[3] JOHNS HOPKINS UNIV HOSP,DIV CARDIOL,BALTIMORE,MD 21287
[4] OHIO STATE UNIV,HEART & LUNG INST,COLUMBUS,OH 43210
来源：
BIOCHEMICAL JOURNAL | 1997年 / 326卷
关键词：
D O I：
10.1042/bj3260017
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We have transiently expressed a dominant negative form of rad (N17rac1) using adenoviral-mediated gene transfer. The level of N17rac1 expression is demonstrated to be proportional to the multiplicity of infection. Expression of N17rac1 in Rat 2 fibroblasts results in cytostatic growth arrest. Cell-cycle analysis demonstrates that cells expressing N17rac1 accumulate in G2/M. These results suggest that rad is required for cell proliferation and provide the first demonstration in mammalian cells of a role for small GTP-binding proteins in the G2/M transition.
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收藏
页码：17 / 20
页数：4
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