H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks. - Wikidata - awgldk - TriplyDB

H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks.

H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks.

http://www.wikidata.org/entity/Q34772965

about

Chk1 suppressed cell death CEP152 is a genome maintenance protein disrupted in Seckel syndrome DNA nucleotide excision repair-dependent signaling to checkpoint activation Transcription Blockage Leads to New Beginnings DNA damage signaling assessed in individual cells in relation to the cell cycle phase and induction of apoptosis Implication of posttranslational histone modifications in nucleotide excision repair Nucleotide excision repair in eukaryotes Mechanism of suppression of chromosomal instability by DNA polymerase POLQ GammaH2AX and cancer An aromatic sensor with aversion to damaged strands confers versatility to DNA repair Cytometry of ATM activation and histone H2AX phosphorylation to estimate extent of DNA damage induced by exogenous agents Oxidative stress induces cell cycle-dependent Mre11 recruitment, ATM and Chk2 activation and histone H2AX phosphorylation.Discovery of a new RNA-containing nuclear structure in UVC-induced apoptotic cells by integrated laser electron microscopy.Kinetics of the UV-induced DNA damage response in relation to cell cycle phase. Correlation with DNA replication.Enhanced H2AX phosphorylation, DNA replication fork arrest, and cell death in the absence of Chk1.A novel and simple micro-irradiation technique for creating localized DNA double-strand breaks.Zebrafish have a competent p53-dependent nucleotide excision repair pathway to resolve ultraviolet B-induced DNA damage in the skin.The nuclear γ-H2AX apoptotic ring: implications for cancers and autoimmune diseases.DNA interstrand crosslink repair in mammalian cells: step by step.Proliferating cell nuclear antigen-dependent rapid recruitment of Cdt1 and CRL4Cdt2 at DNA-damaged sites after UV irradiation in HeLa cells.Halofuginone enhances the radiation sensitivity of human tumor cell lines PI 3 kinase related kinases-independent proteolysis of BRCA1 regulates Rad51 recruitment during genotoxic stress in human cells.Creating localized DNA double-strand breaks with microirradiation.A minority of foci or pan-nuclear apoptotic staining of gammaH2AX in the S phase after UV damage contain DNA double-strand breaks.The DNA damage response kinases DNA-dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated (ATM) Are stimulated by bulky adduct-containing DNA.Transcription inhibition by DRB potentiates recombinational repair of UV lesions in mammalian cells.Analysis of individual molecular events of DNA damage response by flow- and image-assisted cytometry Expression of arf tumor suppressor in spermatogonia facilitates meiotic progression in male germ cells.DNA damage and DNA damage responses in THP-1 monocytes after exposure to spores of either Stachybotrys chartarum or Aspergillus versicolor or to T-2 toxin.Wip1 directly dephosphorylates gamma-H2AX and attenuates the DNA damage response Rad3 decorates critical chromosomal domains with gammaH2A to protect genome integrity during S-Phase in fission yeast.Mechanisms of chromosomal instability in melanoma.Initiation of DNA interstrand cross-link repair in mammalian cells.NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites KML001, a telomere-targeting drug, sensitizes glioblastoma cells to temozolomide chemotherapy and radiotherapy through DNA damage and apoptosis.UV-induced histone H2AX phosphorylation and DNA damage related proteins accumulate and persist in nucleotide excision repair-deficient XP-B cells Starvation-induced activation of ATM/Chk2/p53 signaling sensitizes cancer cells to cisplatin MDC1 cleavage by caspase-3: a novel mechanism for inactivating the DNA damage response during apoptosis.Transcription-coupled DNA double-strand breaks are mediated via the nucleotide excision repair and the Mre11-Rad50-Nbs1 complex Stepping up melanocytes to the challenge of UV exposure.

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H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks.

http://www.wikidata.org/entity/Q34772965

description

2006 nî lūn-bûn

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2006 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի հունիսին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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type

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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H2AX phosphorylation within th ...... not DNA double-strand breaks.

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P2093

Eli Hefner

http://www.w3.org/2001/XMLSchema#string

James E Cleaver

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Luzviminda Feeney

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Thomas M Marti

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Valerie Natale

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P2860

DNA end-joining catalyzed by human cell-free extracts

UV-induced replication arrest in the xeroderma pigmentosum variant leads to DNA double-strand breaks, gamma -H2AX formation, and Mre11 relocalization

Megabase chromatin domains involved in DNA double-strand breaks in vivo

DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139

Initiation of DNA fragmentation during apoptosis induces phosphorylation of H2AX histone at serine 139

A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage

ATM phosphorylates histone H2AX in response to DNA double-strand breaks

Histone H2AX is phosphorylated in an ATR-dependent manner in response to replicational stress

Genomic instability in mice lacking histone H2AX

53BP1 is required for class switch recombination.

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103

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16788066

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phosphorylation

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1502549

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