BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids. - Wikidata - awgldk - TriplyDB

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

http://www.wikidata.org/entity/Q42870831

about

Noncanonical views of homology-directed DNA repair Genome-wide high-resolution mapping of chromosome fragile sites in Saccharomyces cerevisiae.CtIP-mediated resection is essential for viability and can operate independently of BRCA1.USP13 regulates the RAP80-BRCA1 complex dependent DNA damage response.BRCA1 controls homologous recombination at Tus/Ter-stalled mammalian replication forks High-resolution mapping of two types of spontaneous mitotic gene conversion events in Saccharomyces cerevisiae DNA damage response factors from diverse pathways, including DNA crosslink repair, mediate alternative end joining.EEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair.Complex Breakpoints and Template Switching Associated with Non-canonical Termination of Homologous Recombination in Mammalian Cells.DEK is required for homologous recombination repair of DNA breaks.Tetratricopeptide repeat factor XAB2 mediates the end resection step of homologous recombination Spatial separation of replisome arrest sites influences homologous recombination quality at a Tus/Ter-mediated replication fork barrier.Human Cell Assays for Synthesis-Dependent Strand Annealing and Crossing over During Double-Strand Break Repair.Deciphering the Code of the Cancer Genome: Mechanisms of Chromosome Rearrangement.The multifaceted influence of histone deacetylases on DNA damage signalling and DNA repair.FANCJ helicase controls the balance between short- and long-tract gene conversions between sister chromatids.Mechanism of tandem duplication formation in BRCA1-mutant cells.BRCA1 gene: function and deficiency.Break induced replication in eukaryotes: mechanisms, functions, and consequences.

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BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

http://www.wikidata.org/entity/Q42870831

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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name

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

@en

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

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type

label

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

@en

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

@nl

prefLabel

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

@en

BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

@nl

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Nature Communications

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BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids.

@en

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Amy Kwok

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

Anyong Xie

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

Bin Huang

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

Gurushankar Chandramouly

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

Nicholas A Willis

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

Ralph Scully

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P2860

Human SIRT6 promotes DNA end resection through CtIP deacetylation

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

Multiple pathways of recombination induced by double-strand breaks in Saccharomyces cerevisiae

Complex landscapes of somatic rearrangement in human breast cancer genomes.

Human CtIP promotes DNA end resection

Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

The DNA Damage Response: Making It Safe to Play with Knives

Improved monomeric red, orange and yellow fluorescent proteins derived from Discosoma sp. red fluorescent protein

Break-induced replication requires all essential DNA replication factors except those specific for pre-RC assembly.

Break-induced replication: a review and an example in budding yeast

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2404

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scholarly article

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10.1038/NCOMMS3404

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4

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2013-01-01T00:00:00Z

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256331535

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1015240695

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23994874

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3838905

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