Waltzing with WASP

被引：51

作者：

Ramesh, N ^{[1
]}

Antón, IM ^{[1
]}

Martínez-Quiles, N ^{[1
]}

Geha, RS ^{[1
]}

机构：

[1] Harvard Univ, Childrens Hosp, Sch Med, Dept Pediat,Div Immunol, Boston, MA 02115 USA

来源：

TRENDS IN CELL BIOLOGY | 1999年 / 9卷 / 01期

关键词：

D O I：

10.1016/S0962-8924(98)01411-1

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Wiskott-Aldrich syndrome (WAS) is an inherited immune deficiency that is marked by eczema, bleeding and recurrent infections. The lymphocytes and platelets of WAS patients display cytoskeletal abnormalities, and their T lymphocytes show a diminished proliferative response to stimulation through the T-cell receptor-CD3 complex (TCR-CD3). The product of the WAS gene, WAS protein (WASP), binds to the small GTPase Cdc42. Small GTPases of the Rho family are crucial for the regulation of the actin-based cytoskeleton. WASP and its relative NWASP might play an important role in regulating the actin cytoskeleton. Since both WASP and NWASP have the potential to bind to multiple proteins, they might serve as a hub to coordinate the redistribution of many cellular signals to the actin cytoskeleton. In this review, the authors discuss the possible role of WASP/NWASP and of the newly described protein WIP, which interacts with WASP and NWASP, in coupling signals from the T-cell receptor to the actin-based cytoskeleton.

引用

页码：15 / 19

页数：5

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