The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not up-regulated following genome damage

Kevin D. Brown, Yael Ziv, Sunanda N. Sadanandan, Luciana Chessa, Francis S. Collins, Yosef Shiloh, Danilo A. Tagle*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

The product of the ataxia-telangiectasia gene (ATM) was identified by using an antiserum developed to a peptide corresponding to the deduced amino acid sequence. The ATM protein is a single, high-molecular weight protein predominantly confined to the nucleus of human fibroblasts, but is present in both nuclear and microsomal fractions from human lymphoblast cells and peripheral blood lymphocytes. ATM protein levels and localization remain constant throughout all stages of the cell cycle. Truncated ATM protein was not detected in lymphoblasts from ataxia-telangiectasia patients homozygous for mutations leading to premature protein termination. Exposure of normal human cells to γ-irradiation and the radiomimetic drug neocarzinostatin had no effect on ATM protein levels, in contrast to a noted rise in p53 levels over the same time interval. These findings are consistent with a role for the ATM protein in ensuring the fidelity of DNA repair and cell cycle regulation following genome damage.

Original languageEnglish
Pages (from-to)1840-1845
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume94
Issue number5
DOIs
StatePublished - 4 Mar 1997

Fingerprint

Dive into the research topics of 'The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not up-regulated following genome damage'. Together they form a unique fingerprint.

Cite this