Break-induced replication is a source of mutation clusters underlying kataegis - Wikidata - awgldk - TriplyDB

Break-induced replication is a source of mutation clusters underlying kataegis

Break-induced replication is a source of mutation clusters underlying kataegis

http://www.wikidata.org/entity/Q34757099

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Mechanisms underlying structural variant formation in genomic disorders Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity The hidden side of unstable DNA repeats: Mutagenesis at a distance Structural variation mutagenesis of the human genome: Impact on disease and evolution.New insights into the generation and role of de novo mutations in health and disease AID/APOBEC deaminases and cancer Hypermutation in human cancer genomes: footprints and mechanisms Genetic instability in budding and fission yeast-sources and mechanisms APOBEC3A and APOBEC3B Preferentially Deaminate the Lagging Strand Template during DNA Replication Disruption of Transcriptional Coactivator Sub1 Leads to Genome-Wide Re-distribution of Clustered Mutations Induced by APOBEC in Active Yeast Genes DNA replication stress mediates APOBEC3 family mutagenesis in breast cancer Ancient genes establish stress-induced mutation as a hallmark of cancer Crystal structure of APOBEC3A bound to single-stranded DNA reveals structural basis for cytidine deamination and specificity.Error-Prone Repair of DNA Double-Strand Breaks.B cell super-enhancers and regulatory clusters recruit AID tumorigenic activity.An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers RPA Stabilization of Single-Stranded DNA Is Critical for Break-Induced Replication.APOBEC-Induced Cancer Mutations Are Uniquely Enriched in Early-Replicating, Gene-Dense, and Active Chromatin Regions Translesion Polymerases Drive Microhomology-Mediated Break-Induced Replication Leading to Complex Chromosomal Rearrangements.Clusters of Multiple Mutations: Incidence and Molecular Mechanisms Whole-Genome Sequencing Reveals Diverse Models of Structural Variations in Esophageal Squamous Cell Carcinoma DNA REPAIR. Mus81 and converging forks limit the mutagenicity of replication fork breakage.The ssDNA Mutator APOBEC3A Is Regulated by Cooperative Dimerization PrimPol prevents APOBEC/AID family mediated DNA mutagenesis Mutation at a distance caused by homopolymeric guanine repeats in Saccharomyces cerevisiae Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis Risks at the DNA Replication Fork: Effects upon Carcinogenesis and Tumor Heterogeneity Deciphering the Code of the Cancer Genome: Mechanisms of Chromosome Rearrangement.DNA replication stress: from molecular mechanisms to human disease.From Mutational Mechanisms in Single Cells to Mutational Patterns in Cancer Genomes.Coupling end resection with the checkpoint response at DNA double-strand breaks.Getting it done at the ends: Pif1 family DNA helicases and telomeres.Eukaryotic DNA Polymerases in Homologous Recombination.Break-induced replication links microsatellite expansion to complex genome rearrangements.Precarious maintenance of simple DNA repeats in eukaryotes.Heat shock proteins stimulate APOBEC-3-mediated cytidine deamination in the hepatitis B virus.Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2.Genome-wide maps of alkylation damage, repair, and mutagenesis in yeast reveal mechanisms of mutational heterogeneity.Short inverted repeats contribute to localized mutability in human somatic cells.Role of the Pif1-PCNA Complex in Pol δ-Dependent Strand Displacement DNA Synthesis and Break-Induced Replication.

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P2860

Break-induced replication is a source of mutation clusters underlying kataegis

http://www.wikidata.org/entity/Q34757099

description

2014 nî lūn-bûn

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2014 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2014 թվականի մայիսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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Break-induced replication is a source of mutation clusters underlying kataegis

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J.CELREP.2014.04.053

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Break-induced replication is a source of mutation clusters underlying kataegis

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Anna Malkova

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Cynthia J Sakofsky

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Steven A Roberts

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P2860

AID/APOBEC cytosine deaminase induces genome-wide kataegis

Mutagenesis, genotoxicity, and repair of 1-methyladenine, 3-alkylcytosines, 1-methylguanine, and 3-methylthymine in alkB Escherichia coli

Mutational processes molding the genomes of 21 breast cancers

Migrating bubble during break-induced replication drives conservative DNA synthesis.

Base damage within single-strand DNA underlies in vivo hypermutability induced by a ubiquitous environmental agent

Genome-wide mutation avalanches induced in diploid yeast cells by a base analog or an APOBEC deaminase

Signatures of mutational processes in human cancer

Hypermutability of damaged single-strand DNA formed at double-strand breaks and uncapped telomeres in yeast Saccharomyces cerevisiae.

Defective resection at DNA double-strand breaks leads to de novo telomere formation and enhances gene targeting

RAD51-dependent break-induced replication differs in kinetics and checkpoint responses from RAD51-mediated gene conversion

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1640-1648

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scholarly article

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5

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7

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Dmitry A. Gordenin

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Michael A Resnick

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2014-05-29T00:00:00Z

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262812005

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24882007

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4274036

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