Spatiotemporal dynamics of DNA repair proteins following laser microbeam induced DNA damage – When is a DSB not a DSB?
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چکیده
منابع مشابه
Structural basis for a novel mechanism of DNA bridging and alignment in eukaryotic DSB DNA repair.
Eukaryotic DNA polymerase mu of the PolX family can promote the association of the two 3'-protruding ends of a DNA double-strand break (DSB) being repaired (DNA synapsis) even in the absence of the core non-homologous end-joining (NHEJ) machinery. Here, we show that terminal deoxynucleotidyltransferase (TdT), a closely related PolX involved in V(D)J recombination, has the same property. We solv...
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DNA double strand breaks (DSBs) are potential lethal lesions but can also lead to chromosome rearrangements, a step promoting carcinogenesis. DNA non-homologous end-joining (NHEJ) is the major DSB rejoining process and occurs in all cell cycle stages. Homologous recombination (HR) can additionally function to repair irradiation-induced two-ended DSBs in G2 phase. In mammalian cells, HR predomin...
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Background: Single nucleotide polymorphisms in 8-oxoguanine DNA glycosylase-1 (OGG1) gene modulates DNA repair capacity and functions as one of the first lines of protective mechanisms against 8-hydroxy-2’-deoxyguanosine (8-OHdG) mutagenicity. OGG1-Cys326 gene polymorphism may decrease DNA repair function, causing oxidative stress due to higher oxidative DNA damage. The main purpose of this stu...
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Comment on: Helchowski CM, et al. Cell Cycle 2013; 12:3749-58; PMID:24107634; http://dx.doi.org/10.4161/cc.26640 Christopher J Bakkenist and Cyrus Vaziri; Departments of Radiation Oncology and Pharmacology and Chemical Biology; University of Pittsburgh School of Medicine; Hillman Cancer Center; Pittsburgh, PA USA; Department of Pathology; University of North Carolina Chapel Hill; Chapel Hill, N...
متن کاملA truncated DNA-damage-signaling response is activated after DSB formation in the G1 phase of Saccharomyces cerevisiae
In Saccharomyces cerevisiae, the DNA damage response (DDR) is activated by the spatio-temporal colocalization of Mec1-Ddc2 kinase and the 9-1-1 clamp. In the absence of direct means to monitor Mec1 kinase activation in vivo, activation of the checkpoint kinase Rad53 has been taken as a proxy for DDR activation. Here, we identify serine 378 of the Rad55 recombination protein as a direct target s...
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ژورنال
عنوان ژورنال: Mutation Research/Genetic Toxicology and Environmental Mutagenesis
سال: 2013
ISSN: 1383-5718
DOI: 10.1016/j.mrgentox.2013.05.006