Cellular localisation of the ataxia-telangiectasia (ATM) gene product and discrimination between mutated and normal forms View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1997-04

AUTHORS

Dianne Watters, Kum Kum Khanna, Heather Beamish, Geoffrey Birrell, Kevin Spring, Padmini Kedar, Magtouf Gatei, Deborah Stenzel, Karen Hobson, Sergei Kozlov, Ning Zhang, Aine Farrell, Jonathan Ramsay, Richard Gatti, Martin Lavin

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 approximately 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. More... »

PAGES

1201037

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1201037

DOI

http://dx.doi.org/10.1038/sj.onc.1201037

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024634861

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9150358


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