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• W2030720512 startingPage "1911" @default.
• W2030720512 abstract "The recently cloned gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) is involved in DNA damage response at different cell cycle checkpoints and also appears to have a wider role in signal transduction. Antibodies prepared against peptides from the predicted protein sequence detected a ∼ 350 kDa protein corresponding to the open reading frame, which was absent in 13/23 A-T homozygotes. Subcellular fractionation, immunoelectronmicroscopy and immunofluorescence showed that the ATM protein is present in the nucleus and cytoplasmic vesicles. This distribution did not change after irradiation. We also provide evidence that ATM protein binds to p53 and this association is defective in A-T cells compatible with the defective p53 response in these cells. These results provide further support for a role for the ATM protein as a sensor of DNA damage and in a more general role in cell signalling, compatible with the broader phenotype of the syndrome." @default.
• W2030720512 created "2016-06-24" @default.
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• W2030720512 date "1997-04-24" @default.
• W2030720512 modified "2023-10-16" @default.
• W2030720512 title "Cellular localisation of the ataxia-telangiectasia (ATM) gene product and discrimination between mutated and normal forms" @default.
• W2030720512 cites W1594700207 @default.
• W2030720512 cites W2119961841 @default.
• W2030720512 doi "https://doi.org/10.1038/sj.onc.1201037" @default.
• W2030720512 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9150358" @default.
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