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Akt regulates drug-induced cell death through Bcl-w downregulation
- Source :
- PLoS ONE, PLoS ONE, Vol 3, Iss 12, p e4070 (2008)
- Publication Year :
- 2008
-
Abstract
- Akt is a serine threonine kinase with a major role in transducing survival signals and regulating proteins involved in apoptosis. To find new interactors of Akt involved in cell survival, we performed a two-hybrid screening in yeast using human full-length Akt c-DNA as bait and a murine c-DNA library as prey. Among the 80 clones obtained, two were identified as Bcl-w. Bcl-w is a member of the Bcl-2 family that is essential for the regulation of cellular survival, and that is up-regulated in different human tumors, such as gastric and colorectal carcinomas. Direct interaction of Bcl-w with Akt was confirmed by immunoprecipitation assays. Subsequently, we addressed the function of this interaction: by interfering with the activity or amount of Akt, we have demonstrated that Akt modulates the amount of Bcl-w protein. We have found that inhibition of Akt activity may promote apoptosis through the downregulation of Bcl-w protein and the consequential reduction in interaction of Bcl-w with pro-apoptotic members of the Bcl-2 family. Our data provide evidence that Bcl-w is a new member of the Akt pathway and that Akt may induce anti-apoptotic signals at least in part through the regulation of the amount and activity of Bcl-w.
- Subjects :
- Programmed cell death
AKT1
lcsh:Medicine
Down-Regulation
Apoptosis
Biology
Transfection
Cell Biology/Cell Signaling
Downregulation and upregulation
Humans
Phosphorylation
lcsh:Science
Protein kinase B
PI3K/AKT/mTOR pathway
Cells, Cultured
Serine/threonine-specific protein kinase
Multidisciplinary
lcsh:R
Cell Biology
Cell Biology/Cellular Death and Stress Responses
Cell biology
lcsh:Q
Signal transduction
Apoptosis Regulatory Proteins
Proto-Oncogene Proteins c-akt
Research Article
HeLa Cells
Signal Transduction
Subjects
Details
- ISSN :
- 19326203
- Volume :
- 3
- Issue :
- 12
- Database :
- OpenAIRE
- Journal :
- PloS one
- Accession number :
- edsair.doi.dedup.....f2b69a301e3d0ad05c995ae793fc4c0d