Evidence for formation of DNA repair centers and dose-response nonlinearity in human cells - Test2 - elhamkhani - TriplyDB

Evidence for formation of DNA repair centers and dose-response nonlinearity in human cells

Evidence for formation of DNA repair centers and dose-response nonlinearity in human cells

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Choreographing the Double Strand Break Response: Ubiquitin and SUMO Control of Nuclear Architecture Evaluating biomarkers to model cancer risk post cosmic ray exposure Characterizing the DNA Damage Response by Cell Tracking Algorithms and Cell Features Classification Using High-Content Time-Lapse Analysis Dynamics between cancer cell subpopulations reveals a model coordinating with both hierarchical and stochastic concepts Adaptive Posttranslational Control in Cellular Stress Response Pathways and Its Relationship to Toxicity Testing and Safety Assessment The new radiobiology: returning to our roots Radiation-induced cancer: a modern view Epidemiology Without Biology: False Paradigms, Unfounded Assumptions, and Specious Statistics in Radiation Science (with Commentaries by Inge Schmitz-Feuerhake and Christopher Busby and a Reply by the Authors)Live cell imaging at the Munich ion microbeam SNAKE - a status report.53BP1 and the LINC Complex Promote Microtubule-Dependent DSB Mobility and DNA Repair Differential miRNA expression profiles in proliferating or differentiated keratinocytes in response to gamma irradiation.Opposite roles for p38MAPK-driven responses and reactive oxygen species in the persistence and resolution of radiation-induced genomic instability.A two-step mechanism for cell fate decision by coordination of nuclear and mitochondrial p53 activities.Recruitment kinetics of DNA repair proteins Mdc1 and Rad52 but not 53BP1 depend on damage complexity.Genetic differences in transcript responses to low-dose ionizing radiation identify tissue functions associated with breast cancer susceptibility Profiling dose-dependent activation of p53-mediated signaling pathways by chemicals with distinct mechanisms of DNA damage Characterizing the radioresponse of pluripotent and multipotent human stem cells.Spatiotemporal dynamics of early DNA damage response proteins on complex DNA lesions.Visualisation of γH2AX foci caused by heavy ion particle traversal; distinction between core track versus non-track damage.Double-strand break repair by interchromosomal recombination: an in vivo repair mechanism utilized by multiple somatic tissues in mammals.A model of photon cell killing based on the spatio-temporal clustering of DNA damage in higher order chromatin structures.Cell biology of mitotic recombination.Radiobiological response to ultra-short pulsed megavoltage electron beams of ultra-high pulse dose rate.Induction and Processing of the Radiation-Induced Gamma-H2AX Signal and Its Link to the Underlying Pattern of DSB: A Combined Experimental and Modelling Study.Double-strand break motions shift radiation risk notions?Cell to Cell Variability of Radiation-Induced Foci: Relation between Observed Damage and Energy Deposition Development of a robust DNA damage model including persistent telomere-associated damage with application to secondary cancer risk assessment.Direct measurement of the 3-dimensional DNA lesion distribution induced by energetic charged particles in a mouse model tissue.The DDR at telomeres lacking intact shelterin does not require substantial chromatin decompaction.Image-Based High Content Screening: Automating the Quantification Process for DNA Damage-Induced Foci.Activation of homologous recombination DNA repair in human skin fibroblasts continuously exposed to X-ray radiation Low doses of X-rays induce prolonged and ATM-independent persistence of γH2AX foci in human gingival mesenchymal stem cells.The chromatin remodeler p400 ATPase facilitates Rad51-mediated repair of DNA double-strand breaks.Resistance of glioblastoma-initiating cells to radiation mediated by the tumor microenvironment can be abolished by inhibiting transforming growth factor-β.Distinct spatiotemporal patterns and PARP dependence of XRCC1 recruitment to single-strand break and base excision repair.The shape of the radiation dose response for DNA double-strand break induction and repair.Contributions of DNA repair and damage response pathways to the non-linear genotoxic responses of alkylating agents.Variations in the Processing of DNA Double-Strand Breaks Along 60-MeV Therapeutic Proton Beams.The role of dose rate in radiation cancer risk: evaluating the effect of dose rate at the molecular, cellular and tissue levels using key events in critical pathways following exposure to low LET radiation Nuclear dynamics of radiation-induced foci in euchromatin and heterochromatin

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P2860

Evidence for formation of DNA repair centers and dose-response nonlinearity in human cells

http://www.wikidata.org/entity/Q24609012

description

2012 nî lūn-bûn

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2012 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2012 թվականի հունվարին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年论文

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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type

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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Evidence for formation of DNA ...... se nonlinearity in human cells

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PNAS.1117849108

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Evidence for formation of DNA ...... se nonlinearity in human cells

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P2093

Alvin T Lo

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

Aris Polyzos

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Aroumougame Asaithamby

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Christopher Pham

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David J Chen

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Jane Dyball

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Joel Swenson

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Mina J Bissell

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PoAn Yang

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Stefan Thalhammer

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P2860

Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses

Computational approach for determining the spectrum of DNA damage induced by ionizing radiation.

Colocalization of multiple DNA double-strand breaks at a single Rad52 repair centre.

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

DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation

DNA double-strand breaks in heterochromatin elicit fast repair protein recruitment, histone H2AX phosphorylation and relocation to euchromatin.

Identification and characterization of a novel and specific inhibitor of the ataxia-telangiectasia mutated kinase ATM

Double-strand breaks in heterochromatin move outside of a dynamic HP1a domain to complete recombinational repair.

Quantitative image analysis of laminin immunoreactivity in skin basement membrane irradiated with 1 GeV/nucleon iron particles.

Image-based modeling reveals dynamic redistribution of DNA damage into nuclear sub-domains.

P304

443-448

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708837

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10.1073/PNAS.1117849108

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2

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109

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Sylvain V. Costes

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2011-12-19T00:00:00Z

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51902502

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22184222

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3258602

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