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The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not up-regulated following genome damage
Author(s) -
Kevin D. Brown,
Yael Ziv,
Sunanda Sadanandan,
Luciana Chessa,
Francis S. Collins,
Yosef Shiloh,
Danilo A. Tagle
Publication year - 1997
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.94.5.1840
Subject(s) - ataxia telangiectasia , microbiology and biotechnology , nuclear protein , biology , gene , gene product , lymphoblast , dna damage , mutation , neocarzinostatin , dna , gene expression , cell culture , genetics , transcription factor
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.

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