Rac2 stimulates Akt activation affecting BAD/Bcl-XL expression while mediating survival and actin function in primary mast cells

被引：142

作者：

Yang, FC

Kapur, R

King, AJ

Tao, W

Kim, C

Borneo, J

Breese, R

Marshall, M

Dinauer, MC

Williams, DA ^{[1
]}

机构：

[1] Indiana Univ, Herman B Wells Ctr Pediat Res, Sch Med, Dept Pediat,Sect Hematol Oncol, Indianapolis, IN 46202 USA

[2] Indiana Univ, Walther Oncol Ctr, Sch Med, Dept Med,Div Hematol Oncol, Indianapolis, IN 46202 USA

[3] Lilly Res Labs, Indianapolis, IN 46285 USA

[4] Indiana Univ, Sch Med, Howard Hughes Med Inst, Indianapolis, IN 46202 USA

来源：

IMMUNITY | 2000年 / 12卷 / 05期

关键词：

D O I：

10.1016/S1074-7613(00)80207-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Mast cells generated from Rac2-deficient (-/-) mice demonstrated defective actin-based functions, including adhesion, migration, and degranulation. Rac2(-/-) mast cells generated lower numbers and less mast cell colonies in response to growth factors and were deficient in vivo. Rac2(-/-) mast cells demonstrated a significant reduction in growth factor-induced survival, which correlated with the lack of activation of Akt and significant changes in the expression of the Bcl-2 family members BAD and Bcl-X-L, in spite of a 3-fold induction of Rac1 protein. These results suggest that Rac2 plays a unique role in multiple cellular functions and describe an essential role for Rac2 in growth factor-dependent survival and expression of BAD/Bcl-X-L.

引用

页码：557 / 568

页数：12

共 71 条

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