BRCA2 is required for homology-directed repair of chromosomal breaks (Q29618799)

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5 November 2019

title

BRCA2 is required for homology-directed repair of chromosomal breaks (English)

2 references

PubMed

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30 April 2017

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5 November 2019

1

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5 November 2019

author name string

A J Pierce

series ordinal

2

1 reference

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5 November 2019

M Jasin

series ordinal

3

1 reference

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language of work or name

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30 April 2017

publication date

1 February 2001

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5 November 2019

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5 November 2019

volume

7

2 references

PubMed

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30 April 2017

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5 November 2019

issue

2

2 references

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30 April 2017

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5 November 2019

page(s)

263-272

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Double-strand break repair deficiency and radiation sensitivity in BRCA2 mutant cancer cells

5 November 2019

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BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement of transcription-coupled DNA repair

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Xrcc3 is required for assembly of Rad51 complexes in vivo

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Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cells

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The BRC repeats in BRCA2 are critical for RAD51 binding and resistance to methyl methanesulfonate treatment

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Expression of BRC repeats in breast cancer cells disrupts the BRCA2-Rad51 complex and leads to radiation hypersensitivity and loss of G(2)/M checkpoint control

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The importance of repairing stalled replication forks

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The XRCC2 and XRCC3 repair genes are required for chromosome stability in mammalian cells

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Role of BRCA2 in control of the RAD51 recombination and DNA repair protein.

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DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation

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Disruption of mouse RAD54 reduces ionizing radiation resistance and homologous recombination.

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Homologous and non-homologous recombination differentially affect DNA damage repair in mice

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A targeted DNA-PKcs-null mutation reveals DNA-PK-independent functions for KU in V(D)J recombination

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Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development

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BRCA1 required for transcription-coupled repair of oxidative DNA damage

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The tumor suppressor gene Brca1 is required for embryonic cellular proliferation in the mouse

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Sister chromatid gene conversion is a prominent double-strand break repair pathway in mammalian cells

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7 January 2021

Mammalian XRCC2 promotes the repair of DNA double-strand breaks by homologous recombination

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The nonhomologous DNA end joining pathway is important for chromosome stability in primary fibroblasts

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Mitotic checkpoint inactivation fosters transformation in cells lacking the breast cancer susceptibility gene, Brca2.

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Homology-directed repair is a major double-strand break repair pathway in mammalian cells

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A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53

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Inactivation of the mouse Brca1 gene leads to failure in the morphogenesis of the egg cylinder in early postimplantation development.

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Targeted mutations of breast cancer susceptibility gene homologs in mice: lethal phenotypes of Brca1, Brca2, Brca1/Brca2, Brca1/p53, and Brca2/p53 nullizygous embryos

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The BRCA2 gene product functionally interacts with p53 and RAD51

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RAB22 and RAB163/mouse BRCA2: proteins that specifically interact with the RAD51 protein

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Loss of heterozygosity induced by a chromosomal double-strand break

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Brca1 controls homology-directed DNA repair

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Involvement of Brca2 in DNA repair

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THE GENETICS OF BREAST CANCER SUSCEPTIBILITY

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Brca2 is coordinately regulated with Brca1 during proliferation and differentiation in mammary epithelial cells

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Characterization of BRCA2: temperature sensitivity of detection and cell-cycle regulated expression

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Brca2 is required for embryonic cellular proliferation in the mouse

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7 January 2021

Homologous recombination and non-homologous end-joining pathways of DNA double-strand break repair have overlapping roles in the maintenance of chromosomal integrity in vertebrate cells

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Antisense inhibition of the RAD51 enhances radiosensitivity

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7 January 2021

Mouse Rad54 affects DNA conformation and DNA-damage-induced Rad51 foci formation

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Consecutive inactivation of both alleles of the pim-1 proto-oncogene by homologous recombination in embryonic stem cells

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Targeted disruption of the Rad51 gene leads to lethality in embryonic mice

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RAD51 interacts with the evolutionarily conserved BRC motifs in the human breast cancer susceptibility gene brca2

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Identifiers

DOI

2 references

Consolidated OpenCitations Corpus – April 2017

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5 November 2019

1 reference

Consolidated OpenCitations Corpus – April 2017

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=11239455

3 references

30 April 2017

Consolidated OpenCitations Corpus – April 2017