Cell Cycle-Regulated Centers of DNA Double-Strand Break Repair
نویسندگان
چکیده
منابع مشابه
DNA Double-Strand Break Repair
ownloade C regulates a myriad of genes controlling cell proliferation, metabolism, differentiation, and apoptosis. lso controls the expression of DNA double-strand break (DSB) repair genes and therefore may be a ial target for anticancer therapy to sensitize cancer cells to DNA damage or prevent genetic instability. report, we studied whether MYC binds to DSB repair gene promoters and modulates...
متن کاملDNA double-strand break repair
The integrity of genomic DNA is crucial for its function. And yet, DNA in living cells is inherently unstable. It is subject to mechanical stress and to many types of chemical modification that may lead to breaks in one or both strands of the double helix. Within the cell, reactive oxygen species generated by normal respiratory metabolism can cause double-strand breaks, as can stalled DNA repli...
متن کاملDouble strand break repair.
DNA double-strand breaks (DSBs) are the most dangerous form of DNA damage and can lead to death, mutation, or malignant transformation. Mammalian cells use three major pathways to repair DSBs: homologous recombination (HR), classical nonhomologous end joining (C-NHEJ), and alternative end joining (A-NHEJ). Cells choose among the pathways by interactions of the pathways with CtIP and 53BP1. HR i...
متن کاملPathways of DNA double-strand break repair during the mammalian cell cycle.
Little is known about the quantitative contributions of nonhomologous end joining (NHEJ) and homologous recombination (HR) to DNA double-strand break (DSB) repair in different cell cycle phases after physiologically relevant doses of ionizing radiation. Using immunofluorescence detection of gamma-H2AX nuclear foci as a novel approach for monitoring the repair of DSBs, we show here that NHEJ-def...
متن کاملHuman CtIP Mediates Cell Cycle Control of DNA End Resection and Double Strand Break Repair*S⃞
In G(0) and G(1), DNA double strand breaks are repaired by nonhomologous end joining, whereas in S and G(2), they are also repaired by homologous recombination. The human CtIP protein controls double strand break (DSB) resection, an event that occurs effectively only in S/G(2) and that promotes homologous recombination but not non-homologous end joining. Here, we mutate a highly conserved cycli...
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ژورنال
عنوان ژورنال: Cell Cycle
سال: 2003
ISSN: 1538-4101,1551-4005
DOI: 10.4161/cc.2.5.483