Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation
Article Abstract:
The gene mutated in ataxia telangiectasia (AT), a rare autosomal recessive disorder, encodes a protein kinase. Cells in AT patients show an abnormal response to ionizing radiation, such as the activation of a nuclear tyrosine kinase encoded by the c-abl proto-oncogene. C-abl in AT patient cells or Atm-deficient mice is not activated by ionizing radiation, and the defect is corrected with ectopic expression of an ATM kinase domain. The c-Abl tyrosine kinase is identified as a phosphorylation target.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1997
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Interaction between ATM protein and c-Abl in response to DNA damage
Article Abstract:
Research has shown that ataxia telangietasia (AT) cells are defective at the G1/S checkpoint following radiation damage. The possibility that AT mutated (ATM) could interact with c-Abl following radiation damage is investigated. ATM was found to bind c-Abl in control cells although not in AT cells, indicating an interaction between the SH3 domain of c-Abl and a DPAPNPPHFP motif of ATM.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1997
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Functional link of BRCA1 and ataxia telangiectasia gene product in DNA damage response
Article Abstract:
Research is presented concerning the hyperphosphorylation and dissociation of the BRCA1-associated protein CtIP9-12 from the familial breast cancer suppressor BRCA1 in the cells of mice.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2000
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