Ataxia telangiectasia: G2 checkpoint and chromosomal damage in proliferating lymphocytes
نویسندگان
چکیده
منابع مشابه
Checkpoint abrogation in G2 compromises repair of chromosomal breaks in ataxia telangiectasia cells.
Checkpoint abrogation in G(2) compromises repair of DNA double-strand breaks (DSB) and confers enhanced G(2) chromosomal radiosensitivity in ataxia telangiectasia (AT) cells. To directly test this hypothesis, we combined calyculin A-induced premature chromosome condensation with conventional cytogenetics to evaluate chromosome damage before and after the G(2) checkpoint in irradiated primary AT...
متن کاملAtaxia telangiectasia-mutated dependent DNA damage checkpoint functions regulate gene expression in human fibroblasts.
The relationships between profiles of global gene expression and DNA damage checkpoint functions were studied in cells from patients with ataxia telangiectasia (AT). Three telomerase-expressing AT fibroblast lines displayed the expected hypersensitivity to ionizing radiation (IR) and defects in DNA damage checkpoints. Profiles of global gene expression in AT cells were determined at 2, 6, and 2...
متن کاملAtaxia telangiectasia-mutated-Rad3-related DNA damage checkpoint signaling pathway triggered by hepatitis B virus infection.
AIM To explore whether acute cellular DNA damage response is induced upon hepatitis B virus (HBV) infection and the effects of the HBV infection. METHODS We incubated HL7702 hepatocytes with HBV-positive serum, mimicking a natural HBV infection process. We used immunoblotting to evaluate protein expression levels in HBV-infected cells or in non-infected cells; immunofluorescence to show ATR f...
متن کاملThe benzene metabolite hydroquinone enhances G2-chromosomal radiosensitivity by inducing a less-efficient G2-M-checkpoint in irradiated lymphocytes.
The hypothesis tested is that a 24-h pre-irradiation-exposure of peripheral blood lymphocytes (PBL) to the benzene metabolite hydroquinone (HQ), at doses that are non-acutely toxic (5 microM), induces a less efficient G2-M-checkpoint and enhances the G2-chromosomal radiosensitivity in a statistically significant manner (p<0.01). A less efficient G2-M-checkpoint may allow the transition of damag...
متن کاملOver Expression of Nucleophosmin and Nucleolin Contributes to the Suboptimal Activation of a G2/M Checkpoint in Ataxia Telangiectasia Fibroblasts.
Ataxia Telangiectasia (AT) cells exhibit suboptimal activation of radiation-induced cell cycle checkpoints despite having a wild type p53 genotype. Reducing or eliminating this delay could restore p53 function and reinstate normal cellular response to genotoxic stress. Here we show that the levels of Nuclephosmin (NPM), NPM phosphorylated at Serine 125, p53, p53 phosphorylated at Serine 15 and ...
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ژورنال
عنوان ژورنال: Mutagenesis
سال: 2001
ISSN: 1464-3804
DOI: 10.1093/mutage/16.5.419