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Elevated Cu/Zn‐SOD exacerbates radiation sensitivity and hematopoietic abnormalities of Atm‐deficient mice
Author(s) -
Peter Yakov,
Rotman Galit,
Lotem Joseph,
Elson Ari,
Shiloh Yosef,
Groner Yoram
Publication year - 2001
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/20.7.1538
Subject(s) - biology , radiation sensitivity , haematopoiesis , cancer research , microbiology and biotechnology , immunology , irradiation , stem cell , physics , nuclear physics
Patients with the genetic disorder ataxia‐telangiectasia (A‐T) display a pleiotropic phenotype that includes neurodegeneration, immunodeficiency, cancer predisposition and hypersensitivity to ionizing radiation. The gene responsible is ATM , and Atm ‐knockout mice recapitulate most features of A‐T. In order to study the involvement of oxidative stress in the A‐T phenotype, we examined mice deficient for Atm and overexpressing human Cu/Zn superoxide dismutase (SOD1). We report that elevated levels of SOD1 exacerbate specific features of the murine Atm‐ deficient phenotype, including abnormalities in hematopoiesis and radiosensitivity. The data are consistent with the possibility that oxidative stress contributes to some of the clinical features associated with the A‐T phenotype.