Cbl-Family Proteins as Regulators of Cytoskeleton-Dependent Phenomena

被引：16

作者：

Lee, Hojin

Tsygankov, Alexander Y.

机构：

[1] Temple Univ, Sch Med, Dept Microbiol & Immunol, Sol Sherry Thrombosis Res Ctr, Philadelphia, PA 19140 USA

[2] Temple Univ, Sch Med, Fels Inst Canc Res, Philadelphia, PA 19140 USA

来源：

JOURNAL OF CELLULAR PHYSIOLOGY | 2013年 / 228卷 / 12期

关键词：

GROWTH-FACTOR RECEPTOR; UBIQUITIN LIGASE ACTIVITY; NIH; 3T3; FIBROBLASTS; DOMAIN BINDING-SITE; C-CBL; NEGATIVE REGULATION; TYROSINE PHOSPHORYLATION; DOWN-REGULATION; EGF RECEPTOR; RHO-GTPASES;

D O I：

10.1002/jcp.24412

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Although the role of Cbl-family proteins as key cellular regulators has been established, phenomena regulated in a Cbl-dependent fashion are multiple and the mechanisms mediating the effects of Cbl proteins are diverse. This finding makes it important to consider different phenomena affected by functions of Cbl proteins individually. Among effects of Cbl on various biological functions there are many cases of regulation of cellular phenomena related to cytoskeletal rearrangements, such as cell adhesion, motility and invasion. Some of these regulatory functions are mediated by adaptor-type interactions of Cbl, especially by Cbl-dependent modulation of phosphatidyl-inositol-3 kinase (PI3K), while others are caused by Cbl-dependent ubiquitylation of various cytoskeletal and regulatory proteins, identified and unidentified. The role of Cbl in regulation of cytoskeleton-dependent cellular functions is discussed in this review. J. Cell. Physiol. 228: 2285-2293, 2013. (c) 2013 Wiley Periodicals, Inc.

引用

页码：2285 / 2293

页数：9

共 206 条

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The Loss of Cbl-Phosphatidylinositol 3-Kinase Interaction Perturbs RANKL-mediated Signaling, Inhibiting Bone Resorption and Promoting Osteoclast Survival [J].