Cdc14A and Cdc14B Redundantly Regulate 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...
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The repair of damaged DNA is a crucial function carried out by all cells. Unrepaired DNA damage can lead to mutation, loss of genetic information, cellular transformation, or cell death. The DNA double strand break (DSB) is one type of damage that must be efficiently and accurately repaired. Two general mechanisms are employed by eukaryotic cells to repair DSBs: homologous recombination and non...
متن کاملPlk1 and CK2 Act in Concert to Regulate Rad51 during DNA Double Strand Break Repair
Homologous recombination (HR) plays an important role in the maintenance of genome integrity. HR repairs broken DNA during S and G2 phases of the cell cycle but its regulatory mechanisms remain elusive. Here, we report that Polo-like kinase 1 (Plk1), which is vital for cell proliferation and is frequently upregulated in cancer cells, phosphorylates the essential Rad51 recombinase at serine 14 (...
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ژورنال
عنوان ژورنال: Molecular and Cellular Biology
سال: 2015
ISSN: 0270-7306,1098-5549
DOI: 10.1128/mcb.00233-15