Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-12-16
pubmed:abstractText
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.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10022120, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10075741, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10359702, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10485710, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10676810, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10811865, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-10958661, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-11087752, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-11448952, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-11994282, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-12094235, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-12486874, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-12668516, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-14523545, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-15120327, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-15289937, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-15389633, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-15505410, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-15684417, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-15963759, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-16751802, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-16785986, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-17110373, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-18276109, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-19713527, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-8550620, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-8650270, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-8663110, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-9414268, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-9444956, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-9721089, http://linkedlifedata.com/resource/pubmed/commentcorrection/19861161-9990038
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1873-3913
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
377-85
pubmed:dateRevised
2011-7-25
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
c-Cbl acts as a mediator of Src-induced activation of the PI3K-Akt signal transduction pathway during TRAIL treatment.
pubmed:affiliation
Institute for Cancer Research, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural