Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
Cells from patients with ataxia telangiectasia are abnormally sensitive to the cytotoxic effect of a tumor promoter, phorbol-12-myristate-13-acetate
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The cellular and molecular responses of ataxia-telangiectasia cells to DNA damage
Cited by (14)
Ataxia-telangiectasia (A-T): An emerging dimension of premature ageing
2017, Ageing Research ReviewsCitation Excerpt :This function of ATM may explain the moderate, variable sensitivity of ATM-deficient cells to a broad range of DNA damaging agents. Among them are UV radiation, alkylating agents, crosslinking agents, hydrogen peroxide, 4-Nitroquinoline 1-oxide, phorbol-12-myristate-13-acetate and topoisomerase 1 poisons (Alagoz et al., 2013; Barfknecht and Little, 1982; Fedier et al., 2003; Hannan et al., 2002; Henderson and Ribecky, 1980; Hoar and Sargent, 1976; Jaspers et al., 1982; Katyal et al., 2014; Lee et al., 2006; Leonard et al., 2004; Mirzayans et al., 1989; Paterson et al., 1976; Scudiero, 1980; Shiloh et al., 1985; Smith et al., 1989; Smith and Paterson, 1980; Speit et al., 2000; Teo and Arlett, 1982; Ward et al., 1994; Yi et al., 1990; Zhang et al., 1996). ATM-deficient cells also exhibit reduced efficiency in resolving Topoisomerase I-DNA covalent intermediates (Alagoz et al., 2013; Katyal et al., 2014).
ATM: Expanding roles as a chief guardian of genome stability
2014, Experimental Cell ResearchCitation Excerpt :This suggests that a spectrum of deficiency exists amongst these cells in coping with a broad array of DNA lesions, not only DSBs. Similar observations were made during the course of our early studies about the sensitivity of A-T cells to DNA damaging agents [98–102] (and unpublished data). An example of documented ATM-mediated pathway in response to UV radiation is the stabilization of ribonucleotide reductase via ATM-mediated phosphorylation of its subunit, p53R2 [103].
Reactive oxygen species, chromosome mutation, and cancer: possible role of clastogenic factors in carcinogenesis
1994, Free Radical Biology and MedicineSensitivity of fibroblasts derived from ataxia-telangiectasia patients to calicheamicin γ<inf>1</inf><sup>I</sup>
1990, Mutation Research LettersAtaxia-telangiectasia: a variant with altered in vitro phenotype of fibroblast cells
1989, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisERS statement on the multidisciplinary respiratory management of ataxia telangiectasia
2015, European Respiratory Review
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Present address: Division of Genetics, The Children's Hospital of Boston, 300 Longwood Avenue, Boston, MA 02115, U.S.A.