Activation of the Abelson tyrosine kinase activity is associated with suppression of apoptosis in hemopoietic cells.
A chromosomal translocation uniquely associated with chronic myeloid leukemia leads to the formation of a chimeric gene, bcr-abl, on the Philadelphia chromosome. The BRC-ABL protein displays an uncontrolled tyrosine kinase activity similar to that seen with the transforming oncogene of the Abelson murine leukemia (ABL) virus (v-abl). An interleukin 3 dependent cell line, IC.DP, has been transfected with a gene encoding a temperature sensitive v-ABL. In the absence of interleukin 3 at the restrictive temperature for ABL tyrosine kinase activity IC.DP cells died via apoptosis. At the permissive temperature ABL tyrosine kinase activity promoted IC.DP cell survival but not proliferation. ABL therefore can specifically suppress apoptosis.
Evans
C A
CA
CRC Molecular and Cellular Pharmacology Group, Manchester University School of Biological Sciences, United Kingdom.
Owen-Lynch
P J
PJ
Whetton
A D
AD
Dive
C
C
D000011:Abelson murine leukemia virus / Q000235:genetics*; D000818:Animals; D017209:Apoptosis; D002460:Cell Line; D004789:Enzyme Activation; D007377:Interleukin-3 / Q000494:pharmacology*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000473:pathology; D008407:Mast Cells / Q000166:cytology* / Q000201:enzymology; D051379:Mice; D016374:Oncogene Proteins v-abl / Q000378:metabolism*; D011505:Protein-Tyrosine Kinases / Q000378:metabolism*
D007377:Interleukin-3; D016374:Oncogene Proteins v-abl; D011505:Protein-Tyrosine Kinases