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ERK signalling and oncogene transformation are not impaired in cells lacking A-Raf
- Source :
- BASE-Bielefeld Academic Search Engine
- Publication Year :
- 2002
- Publisher :
- Springer Science and Business Media LLC, 2002.
-
Abstract
- Previous studies have indicated an important role for the Raf family of protein kinases in controlling cellular responses to extracellular stimuli and activated oncogenes, through their ability to activate the MEK/ERKs. To investigate the specific role of A-Raf in this process we generated A-Raf deficient mouse embryonic fibroblasts (MEFs) and embryonic stem (ES) cells by gene targeting and characterized their ability to undergo proliferation, differentiation, apoptosis, ERK activation, and transformation by oncogenic Ras and Src. The A-Raf deficient cells are not disrupted for any of these processes, despite the fact that this protein is normally expressed at high levels in both cell types. This implies either that A-Raf plays no role in MEK/ERK activation, that its function is fully compensated by other Raf proteins or MEK kinases or that its role in MEK/ERK activation is highly tissue-specific. Interestingly, B-Raf and Raf-1 activity towards MEK as measured by the immunoprecipitation kinase cascade assay are both significantly increased in the A-Raf deficient MEFs.
- Subjects :
- Male
MAPK/ERK pathway
Cancer Research
MAP Kinase Signaling System
Cellular differentiation
Blotting, Western
Apoptosis
Biology
Polymerase Chain Reaction
Proto-Oncogene Proteins A-raf
Cell Line
Mice
Genetics
Animals
Cell Lineage
Protein kinase A
Molecular Biology
Oncogene
Kinase
Stem Cells
Teratoma
Cell Differentiation
Oncogenes
Fibroblasts
Cell biology
Enzyme Activation
Proto-Oncogene Proteins c-raf
Genes, src
Cell Transformation, Neoplastic
Genes, ras
Immunology
Mitogen-Activated Protein Kinases
Signal transduction
Stem cell
Cell Division
Proto-oncogene tyrosine-protein kinase Src
Subjects
Details
- ISSN :
- 14765594 and 09509232
- Volume :
- 21
- Database :
- OpenAIRE
- Journal :
- Oncogene
- Accession number :
- edsair.doi.dedup.....da567a71eba03387c5a7819ffa0ba75c