gammaH2AX foci analysis for monitoring DNA double-strand break repair: strengths, limitations and optimization. - Wikidata - wikimedia - TriplyDB

gammaH2AX foci analysis for monitoring DNA double-strand break repair: strengths, limitations and optimization.

gammaH2AX foci analysis for monitoring DNA double-strand break repair: strengths, limitations and optimization.

http://www.wikidata.org/entity/Q39742371

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APLF promotes the assembly and activity of non-homologous end joining protein complexes Multiple roles of ATM in monitoring and maintaining DNA integrity Targeting abnormal DNA repair in therapy-resistant breast cancers MicroRNA-138 modulates DNA damage response by repressing histone H2AX expression Translational Research to Improve the Efficacy of Carbon Ion Radiotherapy: Experience of Gunma University Evaluating biomarkers to model cancer risk post cosmic ray exposure Markers of cellular senescence. Telomere shortening as a marker of cellular senescence DNA damage and repair in plants - from models to crops When heat casts a spell on the DNA damage checkpoints Sources of DNA double-strand breaks and models of recombinational DNA repair Use of the γ-H2AX assay to monitor DNA damage and repair in translational cancer research TDP2-dependent non-homologous end-joining protects against topoisomerase II-induced DNA breaks and genome instability in cells and in vivo Visualization of complex DNA double-strand breaks in a tumor treated with carbon ion radiotherapy.Preclinical study of the DNA repair inhibitor Dbait in combination with chemotherapy in colorectal cancer Interference in DNA replication can cause mitotic chromosomal breakage unassociated with double-strand breaks DNA ligases I and III cooperate in alternative non-homologous end-joining in vertebrates INMAP overexpression inhibits cell proliferation, induces genomic instability and functions through p53/p21 pathways Deregulation of DNA double-strand break repair in multiple myeloma: implications for genome stability Targeting the DNA double strand break repair machinery in prostate cancer Evaluation of Severe Combined Immunodeficiency and Combined Immunodeficiency Pediatric Patients on the Basis of Cellular Radiosensitivity.Comprehensive profiling of radiosensitive human cell lines with DNA damage response assays identifies the neutral comet assay as a potential surrogate for clonogenic survival.DNA double-strand breaks induced by cavitational mechanical effects of ultrasound in cancer cell lines.Regulation of pairing between broken DNA-containing chromatin regions by Ku80, DNA-PKcs, ATM, and 53BP1 ATM and ATR activities maintain replication fork integrity during SV40 chromatin replication.Imaging the DNA damage response with PET and SPECT The Effect of VPA on Increasing Radiosensitivity in Osteosarcoma Cells and Primary-Culture Cells from Chemical Carcinogen-Induced Breast Cancer in Rats.DNA-SCARS: distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion Homeostatic control of polo-like kinase-1 engenders non-genetic heterogeneity in G2 checkpoint fidelity and timing.The dominant role of proofreading exonuclease activity of replicative polymerase ε in cellular tolerance to cytarabine (Ara-C)Identification of the elementary structural units of the DNA damage response.DNA breaks and chromosomal aberrations arise when replication meets base excision repair.Difference in the relative biological effectiveness and DNA damage repair processes in response to proton beam therapy according to the positions of the spread out Bragg peak.Gimeracil, an inhibitor of dihydropyrimidine dehydrogenase, inhibits the early step in homologous recombination.High mitochondrial priming sensitizes hESCs to DNA-damage-induced apoptosis.Inducible response required for repair of low-dose radiation damage in human fibroblasts.DNA-damage accumulation and replicative arrest in Hutchinson-Gilford progeria syndrome Development and validation of 'AutoRIF': software for the automated analysis of radiation-induced foci.Endogenously induced DNA double strand breaks arise in heterochromatic DNA regions and require ataxia telangiectasia mutated and Artemis for their repair.Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.Opposite roles for p38MAPK-driven responses and reactive oxygen species in the persistence and resolution of radiation-induced genomic instability.

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P2860

gammaH2AX foci analysis for monitoring DNA double-strand break repair: strengths, limitations and optimization.

http://www.wikidata.org/entity/Q39742371

description

2010 nî lūn-bûn

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

@zh-my

2010年学术文章

@zh-sg

2010年學術文章

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2010年學術文章

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2010年學術文章

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name

gammaH2AX foci analysis for mo ...... limitations and optimization.

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gammaH2AX foci analysis for mo ...... limitations and optimization.

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type

label

gammaH2AX foci analysis for mo ...... limitations and optimization.

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gammaH2AX foci analysis for mo ...... limitations and optimization.

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prefLabel

gammaH2AX foci analysis for mo ...... limitations and optimization.

@en

gammaH2AX foci analysis for mo ...... limitations and optimization.

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gammaH2AX foci analysis for mo ...... limitations and optimization.

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Aaron A Goodarzi

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Andrea Beucher

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Anna Fisher

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Atsushi Shibata

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Markus Löbrich

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scholarly article

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20139725

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