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Open AccessJournal ArticleDOI

Purified human BRCA2 stimulates RAD51-mediated recombination

Ryan B. Jensen, +2 more
- 07 Oct 2010 - 
- Vol. 467, Iss: 7316, pp 678-683
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TLDR
The purification of full-length BRCA2 is reported and it is shown that it both binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA).
Abstract
Mutation of the breast cancer susceptibility gene, BRCA2, leads to breast and ovarian cancers. Mechanistic insight into the functions of human BRCA2 has been limited by the difficulty of isolating this large protein (3,418 amino acids). Here we report the purification of full-length BRCA2 and show that it both binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). BRCA2 acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis. BRCA2 does not anneal ssDNA complexed with RPA, implying it does not directly function in repair processes that involve ssDNA annealing. Our findings show that BRCA2 is a key mediator of homologous recombination, and they provide a molecular basis for understanding how this DNA repair process is disrupted by BRCA2 mutations, which lead to chromosomal instability and cancer.

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Journal ArticleDOI

BRCA1 and BRCA2: different roles in a common pathway of genome protection

TL;DR: The links between the two proteins must exist to explain the marked similarity of human cancer susceptibility that arises with germline mutations in these genes, and the proteins work in concert to protect the genome from double-strand DNA damage during DNA replication.
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Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications

TL;DR: How the development of various complementary methodologies has provided valuable insights into the spatiotemporal dynamics of DDR protein assembly/disassembly at sites of DNA strand breaks in eukaryotic cells is outlined.
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Double-strand break repair-independent role for BRCA2 in blocking stalled replication fork degradation by MRE11

TL;DR: Using single-molecule DNA fiber analysis, it is shown that nascent replication tracts created before fork stalling with hydroxyurea are degraded in the absence of BRCA2 but are stable in wild-type cells.
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DNA interstrand crosslink repair and cancer.

TL;DR: Understanding how the FA pathway links nucleases, helicases and other DNA-processing enzymes should lead to more targeted uses of ICL-inducing agents in cancer treatment and could provide novel insights into drug resistance.
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DNA repair dysregulation from cancer driver to therapeutic target

TL;DR: First, to prevent or reverse therapy resistance; and second, using a synthetic lethal approach to specifically kill cancer cells that are dependent on a compensatory DNA repair pathway for survival in the context of cancer-associated oxidative and replicative stress are tested.
References
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Journal ArticleDOI

Genetic instabilities in human cancers

TL;DR: There is now evidence that most cancers may indeed be genetically unstable, but that the instability exists at two distinct levels, and recognition and comparison of these instabilities are leading to new insights into tumour pathogenesis.
Journal ArticleDOI

Identification of the breast cancer susceptibility gene BRCA2

TL;DR: The identification of a gene in which six different germline mutations in breast cancer families that are likely to be due to BRCA2 are detected, and results indicate that this is the BRC a2 gene.
Journal ArticleDOI

Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2

TL;DR: Developmental arrest in Brca2-deficient embryos, their radiation sensitivity, and the association of Brca1 with Rad51 indicate that Brca 2 may be an essential cofactor in the Rad51-dependent DNA repair of double-strand breaks, thereby explaining the tumour-suppressor function of BrCA2.
Journal ArticleDOI

BRCA2 is required for homology-directed repair of chromosomal breaks.

TL;DR: It is proposed that impaired homology-directed repair caused by BRCA2 deficiency leads to chromosomal instability and, possibly, tumorigenesis, through lack of repair or misrepair of DNA damage.
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