Journal
CYTOGENETIC AND GENOME RESEARCH
Volume 107, Issue 3-4, Pages 256-262Publisher
KARGER
DOI: 10.1159/000080603
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Funding
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD039384] Funding Source: NIH RePORTER
- NICHD NIH HHS [R01 HD39384] Funding Source: Medline
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ATM, the protein product of the gene mutated in the human autosomal recessive disorder ataxia telangiectasia, is involved in detection of double strand breaks (DSBs) and is a key component of the damage surveillance network of cell cycle proteins. In somatic cells ATM phosphorylates many other proteins including p53, an important regulator of cell cycle control. Mice deficient for Atm are male sterile with arrest and apoptosis occurring at testis epithelial stage IV, which in normal spermatocytes corresponds to mid-pachynema. Unlike the situation in somatic cells, we find no evidence that disruption of the Trp53 (p53) gene, or its down-stream target Cdkn1a (p21/ Cip1) results in even a partial rescue of the Atm defect. Copyright (C) 2004 S. Karger AG, Basel.
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