Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-05

AUTHORS

R Baskaran, L D Wood, L L Whitaker, C E Canman, S E Morgan, Y Xu, C Barlow, D Baltimore, A Wynshaw-Boris, M B Kastan, J Y Wang

ABSTRACT

Ataxia telangiectasia (AT) is a rare human autosomal recessive disorder with pleiotropic phenotypes, including neuronal degeneration, immune dysfunction, premature ageing and increased cancer risk. The gene mutated in AT, ATM, encodes a putative lipid or protein kinase. Most of the human AT patient phenotypes are recapitulated in Atm-deficient mice. Cells derived from Atm-/- mice, like those from AT patients, exhibit abnormal response to ionizing radiation. One of the known responses to ionizing radiation is the activation of a nuclear tyrosine kinase encoded by the c-abl proto-oncogene. Ionizing radiation does not activate c-Abl in cells from AT patients or in thymocytes or fibroblasts from the Atm-deficient mice. Ectopic expression of a functional ATM kinase domain corrects this defect, as it phosphorylates the c-Abl tyrosine kinase in vitro at Ser 465, leading to the activation of c-Abl. A mutant c-Abl with Ser 465 changed to Ala 465 is not activated by ionizing radiation or ATM kinase in vivo. These findings identify the c-Abl tyrosine kinase as a downstream target of phosphorylation and activation by the ATM kinase in the cellular response to ionizing radiation. More... »

PAGES

516-519

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/387516a0

DOI

http://dx.doi.org/10.1038/387516a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031716517

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9168116


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