期刊
CELLULAR SIGNALLING
卷 19, 期 7, 页码 1602-1609出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2007.02.008
关键词
Abi-1; Cbl; EGF receptor; endocytosis; Abl kinase
类别
资金
- NCI NIH HHS [R01 CA070940, CA 70940, R01 CA070940-12, R01 CA070940-11, R01 CA070940-13] Funding Source: Medline
The Abl-interactor (Abi) proteins are involved in the regulation of actin polymerization and have recently been shown to modulate epidermal growth factor receptor (EGFR) endocytosis. Here we describe the identification of a novel complex between Abi-1 and the Cbl ubiquitin ligase that is induced by stimulation with EGE Notably, an Abi-1 mutant lacking the SH3 domain (Delta SH3) fails to interact with Cbl and inhibits EGFR internalization. We show that expression of the Abi-1 Delta SH3 mutant inhibits Cbl accumulation at the plasma membrane after EGF treatment. We have previously shown that the oncogenic Abl tyrosine kinase inhibits EGFR internalization. Here we report that the oncogenic Abl kinase disrupts the EGF-inducible Abi-1/Cbl complex, highlighting the importance of Abl kinases and downstream effectors in the regulation of EGFR internalization. Thus, our work reveals a new role for oncogenic Abl tyrosine kinases in the regulation of the Abi-1/Cbl protein complex and uncovers a role for the Abi-1/Cbl complex in the regulation of EGFR endocytosis. (c) 2007 Elsevier Inc. All rights reserved.
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