Limiting the persistence of a chromosome break diminishes its mutagenic potential. - Wikidata - wikimedia - TriplyDB

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

http://www.wikidata.org/entity/Q33510904

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PIAS3 promotes homology‑directed repair and distal non‑homologous end joining DNA double-strand break repair pathway choice and cancer Repair of strand breaks by homologous recombination Targeted gene disruption to cure HIV Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis ATM limits incorrect end utilization during non-homologous end joining of multiple chromosome breaks Repair at single targeted DNA double-strand breaks in pluripotent and differentiated human cells Coupling endonucleases with DNA end-processing enzymes to drive gene disruption.An RNF168 fragment defective for focal accumulation at DNA damage is proficient for inhibition of homologous recombination in BRCA1 deficient cells.High frequency targeted mutagenesis using engineered endonucleases and DNA-end processing enzymes.TGFβ induces "BRCAness" and sensitivity to PARP inhibition in breast cancer by regulating DNA-repair genes The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line.Defining a genotoxic profile with mouse embryonic stem cells Trex2 enables spontaneous sister chromatid exchanges without facilitating DNA double-strand break repair.DNA damage response factors from diverse pathways, including DNA crosslink repair, mediate alternative end joining.Correct end use during end joining of multiple chromosomal double strand breaks is influenced by repair protein RAD50, DNA-dependent protein kinase DNA-PKcs, and transcription context.Heavy Metal Exposure Influences Double Strand Break DNA Repair Outcomes.EXO1 is critical for embryogenesis and the DNA damage response in mice with a hypomorphic Nbs1 allele.Tracking genome engineering outcome at individual DNA breakpoints Multifaceted role of TREX2 in the skin defense against UV-induced skin carcinogenesis.RING finger nuclear factor RNF168 is important for defects in homologous recombination caused by loss of the breast cancer susceptibility factor BRCA1 BRCA1-Ku80 protein interaction enhances end-joining fidelity of chromosomal double-strand breaks in the G1 phase of the cell cycle Heterozygous PALB2 c.1592delT mutation channels DNA double-strand break repair into error-prone pathways in breast cancer patients.Contribution of canonical nonhomologous end joining to chromosomal rearrangements is enhanced by ATM kinase deficiency.In vitro Inactivation of Latent HSV by Targeted Mutagenesis Using an HSV-specific Homing Endonuclease Collaboration and competition between DNA double-strand break repair pathways.Redesign of extensive protein-DNA interfaces of meganucleases using iterative cycles of in vitro compartmentalization.Chromosomal Rearrangements in Cancer: Detection and potential causal mechanisms.Salient Features of Endonuclease Platforms for Therapeutic Genome Editing MAD2L2 controls DNA repair at telomeres and DNA breaks by inhibiting 5' end resection Regulation of Single-Strand Annealing and its Role in Genome Maintenance.BRCA1 requirement for the fidelity of plasmid DNA double-strand break repair in cultured breast epithelial cells.Live imaging of induced and controlled DNA double-strand break formation reveals extremely low repair by homologous recombination in human cells.MRE11 stability is regulated by CK2-dependent interaction with R2TP complex.Double deficiency of Trex2 and DNase1L2 nucleases leads to accumulation of DNA in lingual cornifying keratinocytes without activating inflammatory responses.Concerted activities of distinct H4K20 methyltransferases at DNA double-strand breaks regulate 53BP1 nucleation and NHEJ-directed repair.Increased single-strand annealing rather than non-homologous end-joining predicts hereditary ovarian carcinoma.C-NHEJ without indels is robust and requires synergistic function of distinct XLF domains.Introduction of Large Sequence Inserts by CRISPR-Cas9 To Create Pathogenicity Mutants in the Multinucleate Filamentous Pathogen Sclerotinia sclerotiorum.Repeat-mediated deletions can be induced by a chromosomal break far from a repeat, but multiple pathways suppress such rearrangements

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Limiting the persistence of a chromosome break diminishes its mutagenic potential.

http://www.wikidata.org/entity/Q33510904

description

2009 nî lūn-bûn

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2009 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@ast

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@en

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

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type

label

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@ast

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@en

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@nl

prefLabel

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@ast

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@en

Limiting the persistence of a chromosome break diminishes its mutagenic potential.

@nl

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JOURNAL.PGEN.1000683

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Limiting the persistence of a chromosome break diminishes its mutagenic potential.

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Amanda Gunn

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Anita Cheng

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Jeremy M Stark

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Nicole Bennardo

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Paul Hasty

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P2860

Alternative-NHEJ is a mechanistically distinct pathway of mammalian chromosome break repair

Nuclear localization and cell cycle-specific expression of CtIP, a protein that associates with the BRCA1 tumor suppressor

The structure-specific endonuclease Ercc1-Xpf is required for targeted gene replacement in embryonic stem cells

Abraxas and RAP80 form a BRCA1 protein complex required for the DNA damage response

Crystal structure and DNA binding functions of ERCC1, a subunit of the DNA structure-specific endonuclease XPF-ERCC1

XRCC3 promotes homology-directed repair of DNA damage in mammalian cells

Eukaryotic DNA ligases: structural and functional insights

Human CtIP promotes DNA end resection

Biochemical and cellular characteristics of the 3' -> 5' exonuclease TREX2

Mre11 Dimers Coordinate DNA End Bridging and Nuclease Processing in Double-Strand-Break Repair

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