Sp1 Facilitates DNA Double-Strand Break Repair through a Nontranscriptional Mechanism
نویسندگان
چکیده
منابع مشابه
ERCC1-XPF endonuclease facilitates DNA double-strand break repair.
ERCC1-XPF endonuclease is required for nucleotide excision repair (NER) of helix-distorting DNA lesions. However, mutations in ERCC1 or XPF in humans or mice cause a more severe phenotype than absence of NER, prompting a search for novel repair activities of the nuclease. In Saccharomyces cerevisiae, orthologs of ERCC1-XPF (Rad10-Rad1) participate in the repair of double-strand breaks (DSBs). R...
متن کاملSaccharomyces cerevisiae Sin3p facilitates DNA double-strand break repair.
There are two main pathways in eukaryotic cells for the repair of DNA double-strand breaks: homologous recombination and nonhomologous end joining. Because eukaryotic genomes are packaged in chromatin, these pathways are likely to require the modulation of chromatin structure. One way to achieve this is by the acetylation of lysine residues on the N-terminal tails of histones. Here we demonstra...
متن کاملDNA 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 کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Molecular and Cellular Biology
سال: 2012
ISSN: 0270-7306,1098-5549
DOI: 10.1128/mcb.00049-12