Back to Search Start Over

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

Authors :
Watters, Dianne
Khanna, Kum Kum
Beamish, Heather
Birrell, Geoffrey
Spring, Kevin
Kedar, Padmini
Gatei, Magtouf
Stenzel, Deborah
Hobson, Karen
Kozlov, Sergei
Zhang, Ning
Farrell, Aine
Ramsay, Jonathan
Gatti, Richard
Lavin, Martin
Source :
Oncogene; 4/24/97, Vol. 14 Issue 16, p1911, 11p
Publication Year :
1997

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. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
09509232
Volume :
14
Issue :
16
Database :
Complementary Index
Journal :
Oncogene
Publication Type :
Academic Journal
Accession number :
8918396
Full Text :
https://doi.org/10.1038/sj.onc.1201037