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.1997 May 29;387(6632):520-3.
doi: 10.1038/387520a0.

Interaction between ATM protein and c-Abl in response to DNA damage

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Interaction between ATM protein and c-Abl in response to DNA damage

T Shafman et al. Nature..

Abstract

The gene mutated in the autosomal recessive disorder ataxia telangiectasia (AT), designated ATM (for 'AT mutated'), is a member of a family of phosphatidylinositol-3-kinase-like enzymes that are involved in cell-cycle control, meiotic recombination, telomere length monitoring and DNA-damage response. Previous results have demonstrated that AT cells are hypersensitive to ionizing radiation and are defective at the G1/S checkpoint after radiation damage. Because cells lacking the protein tyrosine kinase c-Abl are also defective in radiation-induced G1 arrest, we investigated the possibility that ATM might interact with c-Abl in response to radiation damage. Here we show that ATM binds c-Abl constitutively in control cells but not in AT cells. Our results demonstrate that the SH3 domain of c-Abl interacts with a DPAPNPPHFP motif (residues 1,373-1,382) of ATM. The results also reveal that radiation-induction of c-Abl tyrosine kinase activity is diminished in AT cells. These findings indicate that ATM is involved in the activation of c-Abl by DNA damage and this interaction may in part mediate radiation-induced G1 arrest.

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  • DNA repair. A sense-abl response?
    Brown L, McCarthy N.Brown L, et al.Nature. 1997 May 29;387(6632):450-1. doi: 10.1038/387450a0.Nature. 1997.PMID:9168102No abstract available.

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