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Titolo:
ATAXIA-TELANGIECTASIA MUTANT PROTEIN ACTIVATES C-ABL TYROSINE KINASE IN RESPONSE TO IONIZING-RADIATION
Autore:
BASKARAN R; WOOD LD; WHITAKER LL; CANMAN CE; MORGAN SE; XU Y; BARLOW C; BALTIMORE D; WYNSHAWBORIS A; KASTAN MB; WANG JYJ;
Indirizzi:
UNIV CALIF SAN DIEGO,DEPT BIOL LA JOLLA CA 92093 UNIV CALIF SAN DIEGO,DEPT BIOL LA JOLLA CA 92093 UNIV CALIF SAN DIEGO,CTR MOL GENET LA JOLLA CA 92093 JOHNS HOPKINS ONCOL CTR BALTIMORE MD 21205 MIT,DEPT BIOL CAMBRIDGE 02139 ENGLAND NIH,NCHGR,LAB GENET DIS RES BETHESDA MD 20892
Titolo Testata:
Nature
fascicolo: 6632, volume: 387, anno: 1997,
pagine: 516 - 519
SICI:
0028-0836(1997)387:6632<516:AMPACT>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLE CHECKPOINT PATHWAY; DNA-DAMAGING AGENTS; CELL-CYCLE; P53; INDUCTION; DOMAIN; GENE; UV;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
25
Recensione:
Indirizzi per estratti:
Citazione:
R. Baskaran et al., "ATAXIA-TELANGIECTASIA MUTANT PROTEIN ACTIVATES C-ABL TYROSINE KINASE IN RESPONSE TO IONIZING-RADIATION", Nature, 387(6632), 1997, pp. 516-519

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(1,2). Most of the human AT patient phenotypes are recapitulated in Atm-deficient mice(3,4). Cells derived from Atm(-/-) mice, like those from AT patients, exhibit abnormal response to ionizing radiation(3,5,6). One of the known responses to ionizing radiation is the activation of a nuclear tyrosine kinase encoded by the c-abl proto-oncogene(7,8). Ionizing radiation does not activate c-Abl in cells from AT patients or in thymocytes or fibroblasts from the Arm-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 toionizing radiation.

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Documento generato il 24/09/20 alle ore 05:11:10