Single-stranded breaks in DNA but not oxidative DNA base damages block transcriptional elongation by RNA polymerase II in HeLa cell nuclear extracts.
about
Defective DNA single-strand break repair in spinocerebellar ataxia with axonal neuropathy-1Cooperation of the Cockayne syndrome group B protein and poly(ADP-ribose) polymerase 1 in the response to oxidative stress.Molecular Basis of Transcriptional Mutagenesis at 8-OxoguaninePCNA monoubiquitylation and DNA polymerase eta ubiquitin-binding domain are required to prevent 8-oxoguanine-induced mutagenesis in Saccharomyces cerevisiae.Cockayne syndrome B protein stimulates apurinic endonuclease 1 activity and protects against agents that introduce base excision repair intermediatesTranscriptional mutagenesis induced by 8-oxoguanine in mammalian cellsTime-Dependent and Organ-Specific Changes in Mitochondrial Function, Mitochondrial DNA Integrity, Oxidative Stress and Mononuclear Cell Infiltration in a Mouse Model of Burn InjuryAbasic sites and strand breaks in DNA cause transcriptional mutagenesis in Escherichia coli.The role of XPC: implications in cancer and oxidative DNA damageNeurotoxic mechanisms of DNA damage: focus on transcriptional inhibition.Transcription blockage by bulky end termini at single-strand breaks in the DNA template: differential effects of 5' and 3' adducts.Expression of a pathogenic mutation of SOD1 sensitizes aprataxin-deficient cells and mice to oxidative stress and triggers hallmarks of premature ageing.Early host cell reactivation of an oxidatively damaged adenovirus-encoded reporter gene requires the Cockayne syndrome proteins CSA and CSB.Preferential repair of oxidized base damage in the transcribed genes of mammalian cellsCombined inadequacies of multiple B vitamins amplify colonic Wnt signaling and promote intestinal tumorigenesis in BAT-LacZxApc1638N mice.RNA polymerase II bypass of oxidative DNA damage is regulated by transcription elongation factorsClinical implications of the basic defects in Cockayne syndrome and xeroderma pigmentosum and the DNA lesions responsible for cancer, neurodegeneration and agingThe role of Cockayne Syndrome group B (CSB) protein in base excision repair and aging.8-Oxoguanine-mediated transcriptional mutagenesis causes Ras activation in mammalian cells.The RECQL4 protein, deficient in Rothmund-Thomson syndrome is active on telomeric D-loops containing DNA metabolism blocking lesionsA ubiquitylation site in Cockayne syndrome B required for repair of oxidative DNA damage, but not for transcription-coupled nucleotide excision repairTranscription-coupled nucleotide excision repair in mammalian cells: molecular mechanisms and biological effects.Acetylation regulates DNA repair mechanisms in human cells.Host cell reactivation of gene expression for an adenovirus-encoded reporter gene reflects the repair of UVC-induced cyclobutane pyrimidine dimers and methylene blue plus visible light-induced 8-oxoguanine.Reactive oxygen species generated by thiopurine/UVA cause irreparable transcription-blocking DNA lesions.Modulation of base excision repair of 8-oxoguanine by the nucleotide sequenceDNA polymerase beta and PARP activities in base excision repair in living cells.Requirement of yeast Rad1-Rad10 nuclease for the removal of 3'-blocked termini from DNA strand breaks induced by reactive oxygen species.The post-replication repair RAD18 and RAD6 genes are involved in the prevention of spontaneous mutations caused by 7,8-dihydro-8-oxoguanine in Saccharomyces cerevisiae.Homology-directed repair of DNA nicks via pathways distinct from canonical double-strand break repair.The Nonbulky DNA Lesions Spiroiminodihydantoin and 5-Guanidinohydantoin Significantly Block Human RNA Polymerase II Elongation in Vitro.Excision of uracil from transcribed DNA negatively affects gene expression.Structure of transcribed chromatin is a sensor of DNA damage.8-Oxo-7,8-dihydroguanine in DNA does not constitute a barrier to transcription, but is converted into transcription-blocking damage by OGG1.Nucleolar disruption and apoptosis are distinct neuronal responses to etoposide-induced DNA damage.Transcription processing at 1,N2-ethenoguanine by human RNA polymerase II and bacteriophage T7 RNA polymeraseGene silencing induced by oxidative DNA base damage: association with local decrease of histone H4 acetylation in the promoter region.Base excision repair and the role of MUTYHDNA 3'-phosphatase activity is critical for rapid global rates of single-strand break repair following oxidative stress.DNA repair and the origins of urinary oxidized 2'-deoxyribonucleosides.
P2860
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P2860
Single-stranded breaks in DNA but not oxidative DNA base damages block transcriptional elongation by RNA polymerase II in HeLa cell nuclear extracts.
description
2004 nî lūn-bûn
@nan
2004 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
name
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@ast
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@en
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@nl
type
label
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@ast
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@en
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@nl
prefLabel
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@ast
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@en
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts.
@nl
P2860
P356
P1476
Single-stranded breaks in DNA ...... in HeLa cell nuclear extracts
@en
P2093
Guang-Ping Shen
Scott D Kathe
P2860
P304
18511-18520
P356
10.1074/JBC.M313598200
P407
P577
2004-02-21T00:00:00Z