Histone acetylation by CBP and p300 at double-strand break sites facilitates SWI/SNF chromatin remodeling and the recruitment of non-homologous end joining factors.
about
Radiation-induced alterations in histone modification patterns and their potential impact on short-term radiation effectsHuman RNF169 is a negative regulator of the ubiquitin-dependent response to DNA double-strand breaksEAF2 suppresses hypoxia-induced factor 1α transcriptional activity by disrupting its interaction with coactivator CBP/p300PARP1-dependent recruitment of KDM4D histone demethylase to DNA damage sites promotes double-strand break repairMetabolic modulation of chromatin: implications for DNA repair and genomic integrityMultiple cellular mechanisms prevent chromosomal rearrangements involving repetitive DNAAcetylation Reader Proteins: Linking Acetylation Signaling to Genome Maintenance and CancerDietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cellsThe RSF1 histone-remodelling factor facilitates DNA double-strand break repair by recruiting centromeric and Fanconi Anaemia proteinsThe SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancersBRMS1 suppresses lung cancer metastases through an E3 ligase function on histone acetyltransferase p300.p38 MAPK- and Akt-mediated p300 phosphorylation regulates its degradation to facilitate nucleotide excision repair.The Arabidopsis SWI2/SNF2 Chromatin Remodeling ATPase BRAHMA Targets Directly to PINs and Is Required for Root Stem Cell Niche Maintenance.Bridging of double-stranded breaks by the nonhomologous end-joining ligation complex is modulated by DNA end chemistry.Chromatin modifications during repair of environmental exposure-induced DNA damage: a potential mechanism for stable epigenetic alterations.PARP3 affects the relative contribution of homologous recombination and nonhomologous end-joining pathways.Chromatin-regulating proteins as targets for cancer therapy.Regulation of the BRCA1 gene by an SRC3/53BP1 complexHistone modifications and DNA double-strand break repair after exposure to ionizing radiations.Learning tasks as a possible treatment for DNA lesions induced by oxidative stress in hippocampal neuronsEssential factors for incompatible DNA end joining at chromosomal DNA double strand breaks in vivo.The DSIF subunits Spt4 and Spt5 have distinct roles at various phases of immunoglobulin class switch recombinationNucleolin participates in DNA double-strand break-induced damage response through MDC1-dependent pathwaySIRT7 promotes genome integrity and modulates non-homologous end joining DNA repair.CBP and p300 histone acetyltransferases contribute to homologous recombination by transcriptionally activating the BRCA1 and RAD51 genes.The histone H2A deubiquitinase USP16 interacts with HERC2 and fine-tunes cellular response to DNA damage.Three-dimensional collagen I promotes gemcitabine resistance in vitro in pancreatic cancer cells through HMGA2-dependent histone acetyltransferase expression.Screen identifies bromodomain protein ZMYND8 in chromatin recognition of transcription-associated DNA damage that promotes homologous recombination.Novel method for site-specific induction of oxidative DNA damage reveals differences in recruitment of repair proteins to heterochromatin and euchromatinSETD2-dependent histone H3K36 trimethylation is required for homologous recombination repair and genome stabilityPre-exposure to ionizing radiation stimulates DNA double strand break end resection, promoting the use of homologous recombination repairRegulation of 53BP1 protein stability by RNF8 and RNF168 is important for efficient DNA double-strand break repairPolynucleotide kinase and aprataxin-like forkhead-associated protein (PALF) acts as both a single-stranded DNA endonuclease and a single-stranded DNA 3' exonuclease and can participate in DNA end joining in a biochemical system.'Relax and Repair' to restrain aging.Organization and dynamics of the nonhomologous end-joining machinery during DNA double-strand break repairATP-dependent chromatin remodeling in the DNA-damage response.Acetyltransferase p300 collaborates with chromodomain helicase DNA-binding protein 4 (CHD4) to facilitate DNA double-strand break repair.L- and D-lactate enhance DNA repair and modulate the resistance of cervical carcinoma cells to anticancer drugs via histone deacetylase inhibition and hydroxycarboxylic acid receptor 1 activationA role for human homologous recombination factors in suppressing microhomology-mediated end joiningThe oncoprotein HBXIP modulates the feedback loop of MDM2/p53 to enhance the growth of breast cancer.
P2860
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P2860
Histone acetylation by CBP and p300 at double-strand break sites facilitates SWI/SNF chromatin remodeling and the recruitment of non-homologous end joining factors.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
2011年學術文章
@zh-hant
name
Histone acetylation by CBP and ...... omologous end joining factors.
@en
Histone acetylation by CBP and ...... omologous end joining factors.
@nl
type
label
Histone acetylation by CBP and ...... omologous end joining factors.
@en
Histone acetylation by CBP and ...... omologous end joining factors.
@nl
prefLabel
Histone acetylation by CBP and ...... omologous end joining factors.
@en
Histone acetylation by CBP and ...... omologous end joining factors.
@nl
P2093
P356
P1433
P1476
Histone acetylation by CBP and ...... omologous end joining factors.
@en
P2093
S Nakajima
P2888
P304
P356
10.1038/ONC.2010.592
P407
P577
2011-01-10T00:00:00Z