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- Title
v-Abl protein tyrosine kinase (PTK) mediated suppression of apoptosis is associated with the up-regulation of Bcl-X<sub>L</sub>.
- Authors
Chen, Quan; Turner, Jonathan; Watson, Alastair JM; Dive, Caroline
- Abstract
We demonstrated previously that the activation of v-Abl protein tyrosine kinase (PTK) in IC.DP murine pre-mast cells resulted in suppression of apoptosis after withdrawal of interleukin 3 (IL-3), that protein kinase C (PKC) translocated to the nucleus 6 h after v-Abl PTK activation and that inhibition of PKC restored apoptosis after IL-3 deprivation in the presence of v-Abl PTK activity. Here we demonstrate that v-Abl PTK activation is followed by an approximately twofold increase in mRNA level of Bcl-XL by 6 h and a corresponding increase in Bcl-XL protein level by 24 h. Bcl-xL RNA and protein decreased in IL-3 deprived cells in the absence of v-Abl PTK activity. Exposure of cells with v-Abl PTK active to the PKC inhbitor calphostin C (125 ng/ml) prevented the increase in Bcl-xL protein and resulted in apoptosis. No changes in Bax or Bcl-2 protein level were noted after IL-3 withdrawal and/or activation of v-Abl PTK. Bak was barely detectable and Bad protein level decreased in cells undergoing apoptosis. The data suggest that suppression of apoptosis by v-Abl PTK in the absence of IL-3 is associated with PKC signalling and the upregulation of Bcl-xL in IC.DP cells.
- Subjects
PROTEIN-tyrosine kinases; APOPTOSIS; TUMOR suppressor genes; GENETIC regulation
- Publication
Oncogene, 1997, Vol 15, Issue 18, p2249
- ISSN
0950-9232
- Publication type
Article
- DOI
10.1038/sj.onc.1201371