Residual gammaH2AX foci as an indication of lethal DNA lesions. - Wikidata - wikimedia - TriplyDB

Residual gammaH2AX foci as an indication of lethal DNA lesions.

Residual gammaH2AX foci as an indication of lethal DNA lesions.

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MutS homologue hMSH5: role in cisplatin-induced DNA damage response DNA damage signaling assessed in individual cells in relation to the cell cycle phase and induction of apoptosis Identification of Small Molecule Proliferating Cell Nuclear Antigen (PCNA) Inhibitor That Disrupts Interactions with PIP-box Proteins and Inhibits DNA Replication Deregulation of DNA double-strand break repair in multiple myeloma: implications for genome stability Cisplatin exposure damages resident stem cells of the mammalian inner ear.Functional Gene Analysis Reveals Cell Cycle Changes and Inflammation in Endothelial Cells Irradiated with a Single X-ray Dose Cellular and cell-free studies of catalytic DNA cleavage by ruthenium polypyridyl complexes containing redox-active intercalating ligands.Regular exercise participation improves genomic stability in diabetic patients: an exploratory study to analyse telomere length and DNA damage.Development and validation of 'AutoRIF': software for the automated analysis of radiation-induced foci.Rad51 inhibition is an effective means of targeting DNA repair in glioma models and CD133+ tumor-derived cells OsSDS is essential for DSB formation in rice meiosis Suberoylanilide hydroxamic acid induces hypersensitivity to radiation therapy in acute myelogenous leukemia cells expressing constitutively active FLT3 mutants.Imaging DNA damage in vivo using gammaH2AX-targeted immunoconjugates RNF8-independent Lys63 poly-ubiquitylation prevents genomic instability in response to replication-associated DNA damage.Suberoylanilide hydroxamic acid (SAHA) enhances olaparib activity by targeting homologous recombination DNA repair in ovarian cancer.Induction and persistence of radiation-induced DNA damage is more pronounced in young animals than in old animals High throughput measurement of γH2AX DSB repair kinetics in a healthy human population The DNA damage mark pH2AX differentiates the cytotoxic effects of small molecule HDAC inhibitors in ovarian cancer cells Ionizing radiation-induced foci persistence screen to discover enhancers of accelerated senescence.Loss of INPP4B causes a DNA repair defect through loss of BRCA1, ATM and ATR and can be targeted with PARP inhibitor treatment.Thymoquinone enhances cisplatin-response through direct tumor effects in a syngeneic mouse model of ovarian cancer Cancer-associated fibroblasts from human NSCLC survive ablative doses of radiation but their invasive capacity is reduced.H2AX phosphorylation at the sites of DNA double-strand breaks in cultivated mammalian cells and tissues.Thailandepsins are new small molecule class I HDAC inhibitors with potent cytotoxic activity in ovarian cancer cells: a preclinical study of epigenetic ovarian cancer therapy Quantitative proteomics profiling of the poly(ADP-ribose)-related response to genotoxic stress.MCPIP is induced by cholesterol and participated in cholesterol-caused DNA damage in HUVEC.Exonuclease 1 (Exo1) is required for activating response to S(N)1 DNA methylating agents.Romidepsin (FK228) combined with cisplatin stimulates DNA damage-induced cell death in ovarian cancer.DNA double-strand break repair: a theoretical framework and its application.Variations in the Processing of DNA Double-Strand Breaks Along 60-MeV Therapeutic Proton Beams.Histone H2AX phosphorylation as a measure of DNA double-strand breaks and a marker of environmental stress and disease activity in lupus.Risk assessment of esophageal adenocarcinoma using γ-H2AX assay Combined effects of C225 and 125-iodine seed radiation on colorectal cancer cells Epigenetic therapy potential of suberoylanilide hydroxamic acid on invasive human non-small cell lung cancer cells Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth.Heterochromatin and the DNA damage response: the need to relax.Isogenic radiation resistant cell lines: development and validation strategies.Complex DNA Damage: A Route to Radiation-Induced Genomic Instability and Carcinogenesis.Panobinostat sensitizes cyclin E high, homologous recombination-proficient ovarian cancer to olaparib.Knockdown of NFBD1/MDC1 enhances chemosensitivity to cisplatin or 5-fluorouracil in nasopharyngeal carcinoma CNE1 cells.

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P2860

Residual gammaH2AX foci as an indication of lethal DNA lesions.

http://www.wikidata.org/entity/Q33522060

description

2010 nî lūn-bûn

@nan

2010 թուականի Յունուարին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունվարին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

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name

Residual gammaH2AX foci as an indication of lethal DNA lesions.

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Residual gammaH2AX foci as an indication of lethal DNA lesions.

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Residual gammaH2AX foci as an indication of lethal DNA lesions.

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type

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Residual gammaH2AX foci as an indication of lethal DNA lesions.

@ast

Residual gammaH2AX foci as an indication of lethal DNA lesions.

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Residual gammaH2AX foci as an indication of lethal DNA lesions.

@nl

prefLabel

Residual gammaH2AX foci as an indication of lethal DNA lesions.

@ast

Residual gammaH2AX foci as an indication of lethal DNA lesions.

@en

Residual gammaH2AX foci as an indication of lethal DNA lesions.

@nl

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Residual gammaH2AX foci as an indication of lethal DNA lesions.

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P2093

C Adriana Banuelos

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

Judit P Banáth

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Peggy L Olive

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Susan H MacPhail

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P2860

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

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

Homologous recombination and cell cycle checkpoints: Rad51 in tumour progression and therapy resistance

GammaH2AX and cancer

Mismatch repair-dependent G2 checkpoint induced by low doses of SN1 type methylating agents requires the ATR kinase.

Perturbed gap-filling synthesis in nucleotide excision repair causes histone H2AX phosphorylation in human quiescent cells.

Chromosome-wide Rad51 spreading and SUMO-H2A.Z-dependent chromosome fixation in response to a persistent DNA double-strand break.

Increased ionizing radiation sensitivity and genomic instability in the absence of histone H2AX

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10.1186/1471-2407-10-4

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