Abl Family Kinases in Development and Disease by Anthony Koleske

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By Anthony Koleske

Abl family members Kinases in improvement and affliction offers an summary of the services of Abl kinfolk kinases in improvement and ailment. This new name discusses the biochemical, genetic, and cellphone organic info that elucidate the mobile roles for those kinases in those processes.

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Activated nuclear ABL can stimulate cell death by transcription-dependent (through p73 and/or RNA polymerase II) mechanism. Activated nuclear ABL can exit to the cytoplasm and stimulate cell death by transcription-independent mechanism. BCR-ABL-transformed cells, supporting the nuclear requirement for activated ABL kinase in inducing cell death. In recent unpublished studies, we have examined the pro-death function of Abl proteins that are either exclusively cytoplasmic (NLS-mutated), exclusively nuclear (Nuc), or shuttling (wild type).

Mouse embryo fibroblasts do not undergo apoptosis in response to IR; hence, the contribution of Abl to IR-induced apoptosis could not be assessed in this experimental system. We have observed reduced apoptotic response to IR with y4^/-knockout mouse thymocytes (Wood LD, Wang JYJ, unpublished observation). ^^ Taken together, the accumulated evidence supports the conclusion that activation of Abl by genotoxins can lead to the stimulation of apoptosis. However, Abl s pro-apoptotic function appears to be dependent on the type of genotoxins and the cellular context.

Inhibition of c-Abl tyrosine kinase activity by filamentous actin. J Biol Chem 2001; 276(29):27104-27110. 50. Lewis J M , Schwartz MA. Integrins regulate the association and phosphorylation of paxillin by c-Abl. J Biol Chem 1998; 273(23):14225-14230. 51. Brasher BB, Van Etten RA. c-Abl has high intrinsic tyrosine kinase activity that is stimulated by mutation of the Src homology 3 domain and by autophosphorylation at two distinct regulatory tyrosines. J Biol Chem 2000; 275(45):35631-35637. 52. Tanis K Q , Veach D , Duewel HS et al.

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