期刊
CELLULAR SIGNALLING
卷 22, 期 3, 页码 377-385出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2009.10.007
关键词
c-Cbl; TRAIL; Src-PI3K-Akt
类别
资金
- NCl [CA1 21395, CA140554, CA1 13263]
- Ministry of Education, Science and Technology [2009-0071809]
- Yonsei University College of Medicine [2009-0113]
- Ministry of Commerce, Industry, and Energy of Korea [99014-05]
- National Research Foundation of Korea [2009-0071809] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
We have previously observed that TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) induces acquired TRAIL resistance by increasing Akt phosphorylation and Bcl-xL expression. In this study, we report that Src, c-Cbl, and PI3K are involved in the phosphorylation of Akt during TRAIL treatment. Data from immunoprecipitation and immunoblotting assay reveal that Src interacts with c-Cbl and PI3K. Data from immune complex kinase assay demonstrate that Src can directly phosphorylate c-CbI and PI3K p85 subunit protein. Data from gene knockdown experiments with an RNA interference (RNAi) technique show that c-Cbl is involved in the interaction between Src and PI3K p85 during TRAIL treatment, playing an important role in TRAIL-induced Akt phosphorylation. Taken together, c-CbI may act as a mediator to regulate the Src-PI3K-Akt signal transduction pathway during TRAIL treatment. (C) 2009 Elsevier Inc. All rights reserved.
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