Vav3 is regulated during the cell cycle and effects cell division

被引：33

作者：

Fujikawa, K

Inoue, Y

Sakai, M

Koyama, Y

Nishi, S

Funada, R

Alt, FW ^{[1
]}

Swat, W

机构：

[1] Harvard Univ, Sch Med, Dept Pediat, Ctr Blood Res, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Genet, Ctr Blood Res, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp, Boston, MA 02115 USA

[4] Hokkaido Univ, Grad Sch Med, Dept Neural Funct, Sapporo, Hokkaido 0608638, Japan

[5] Hokkaido Univ, Grad Sch Med, Dept Biochem, Sapporo, Hokkaido 0608638, Japan

[6] Hokkaido Univ, Grad Sch Agr, Lab Wood Biol, Sapporo, Hokkaido 0608589, Japan

[7] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2002年 / 99卷 / 07期

关键词：

D O I：

10.1073/pnas.052715699

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：

Vav3 is a member of the family of guanine nucleotide exchange factors implicated in the regulation of Rho GTPases. Although the exact in vivo function of Vav3 is unknown, evidence from several studies indicates a role distinct from Vav2 or Vav1. Here we report that the expression of Vav3 is regulated during the cell cycle. Strikingly, Vav3 was transiently up-regulated in HeLa cells during mitosis, whereas enforced expression of Vav3 perturbed cytokinesis and led to the appearance of multinucleated cells. These effects of Vav3 were RhoA-dependent, required phosphorylation of the regulatory tyrosine 173, but were not enhanced by N-terminal truncations. Thus, this report establishes that expression of Vav3 is strictly regulated in a cell cycle-dependent manner and implicates Vav3 in the control of cytokinesis.

引用

页码：4313 / 4318

页数：6

共 18 条

[1] Structural basis for relief of autoinhibition of the Dbl homology domain of proto-oncogene Vav by tyrosine phosphorylation [J].