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c-Cbl acts as a mediator of Src-induced activation of the PI3K-Akt signal transduction pathway during TRAIL treatment.

Authors
 Jae J. Song  ;  Joo-Hang Kim  ;  Bo K. Sun  ;  Marco A. Alcala Jr  ;  David L. Bartlett  ;  Yong J. Lee 
Citation
 CELLULAR SIGNALLING, Vol.22(3) : 377-385, 2010 
Journal Title
 CELLULAR SIGNALLING 
ISSN
 0898-6568 
Issue Date
2010
MeSH
Caspase 8/genetics ; Caspase 8/metabolism ; Cell Line, Tumor ; Humans ; Phosphatidylinositol 3-Kinases/metabolism* ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-cbl/genetics ; Proto-Oncogene Proteins c-cbl/metabolism ; Proto-Oncogene Proteins c-cbl/physiology* ; Proto-Oncogene Proteins pp60(c-src)/metabolism* ; RNA, Small Interfering/metabolism ; Signal Transduction* ; TNF-Related Apoptosis-Inducing Ligand/pharmacology*
Keywords
c-Cbl ; TRAIL ; Src-PI3K-Akt
Abstract
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-Cbl 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-Cbl may act as a mediator to regulate the Src-PI3K-Akt signal transduction pathway during TRAIL treatment.
Files in This Item:
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DOI
10.1016/j.cellsig.2009.10.007
Appears in Collections:
5. Research Institutes (연구소) > Institute for Cancer Research (암연구소) > 1. Journal Papers
Yonsei Authors
Song, Jae Jin(송재진) ORCID logo https://orcid.org/0000-0001-8183-9550
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/100425
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