DNA damage induced Pol η recruitment takes place independently of the cell cycle phase
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چکیده
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Cell cycle phase recovery from bleomycin-induced potentially lethal damage.
Mammalian cells treated during mitosis with the anticancer drug bleomycin cannot recover from potentially lethal damage. G1- and S-phase cells treated in a similar manner can recover. In synchronized G1- and S-phase cells, and in asynchronous and nondividing populations, the final survival values of recovered cells have always been found to be greater than 0.2. These data suggest that a certain...
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Although it is well established that plant seeds treated with high doses of gamma radiation arrest development as seedlings, the cause of this arrest is unknown. The uvh1 mutant of Arabidopsis is defective in a homolog of the human repair endonuclease XPF, and uvh1 mutants are sensitive to both the toxic effects of UV and the cytostatic effects of gamma radiation. Here we find that gamma irradi...
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In response to DNA damage, ataxia-telangiectasia mutant and ataxia-telangiectasia and Rad-3 activate p53, resulting in either cell cycle arrest or apoptosis. We report here that DNA damage stimuli, including etoposide (ETOP), adriamycin (ADR), ionizing irradiation (IR), and ultraviolet irradiation (UV) activate ERK1/2 (ERK) mitogen-activated protein kinase in primary (MEF and IMR90), immortaliz...
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The Fanconi anemia (FA)-BRCA pathway mediates repair of DNA interstrand crosslinks. The FA core complex, a multi-subunit ubiquitin ligase, participates in the detection of DNA lesions and monoubiquitinates two downstream FA proteins, FANCD2 and FANCI (or the ID complex). However, the regulation of the FA core complex itself is poorly understood. Here we show that the FA core complex proteins ar...
متن کاملc-Myc is necessary for DNA damage-induced apoptosis in the G(2) phase of the cell cycle.
The c-myc proto-oncogene encodes a transcription factor that participates in the regulation of cellular proliferation, differentiation, and apoptosis. Ectopic overexpression of c-Myc has been shown to sensitize cells to apoptosis. We report here that cells lacking c-Myc activity due to disruption of the c-myc gene by targeted homologous recombination are defective in DNA damage-initiated apopto...
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ژورنال
عنوان ژورنال: Cell Cycle
سال: 2009
ISSN: 1538-4101,1551-4005
DOI: 10.4161/cc.8.20.9836