The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Double-Strand Break Repair-Independent Role for BRCA2 in Blocking Stalled Replication Fork Degradation by MRE11
Open accessAbstract
SUMMARY Breast cancer suppressor BRCA2 is critical for maintenance of genomic integrity and resistance to agents that damage DNA or collapse replication forks, presumably through homology-directed repair of double-strand breaks (HDR). Using single-molecule DNA fiber analysis, we show here that nascent replication tracts created before fork stalling with hydroxyurea are degraded in the absence of BRCA2 but are stable in wild-type cells. BRCA2 mutational analysis reveals that a conserved C-terminal site, involved in stabilizing RAD51 filaments but not in loading RAD51 onto DNA, is essential for this fork protection but dispensable for HDR. RAD51 filament disruption in wild-type cells phenocopies BRCA2 deficiency. BRCA2 prevents chromosomal aberrations upon replication stalling, which are alleviated by inhibition of MRE11, the nuclease responsible for this novel fork instability. Thus, BRCA2 prevents rather than repairs nucleolytic lesions at stalled replication forks to maintain genomic integrity, and hence likely suppresses tumorigenesis through this novel replication-specific function.
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Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
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Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
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Genomic instability — an evolving hallmark of cancer
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Simple and highly efficient BAC recombineering using galK selection
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Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers
Sakai, W., Swisher, E. M., Karlan, B. Y., Agarwal, M. K., Higgins, J., Friedman, C., Villegas, E., Jacquemont, C., Farrugia, D. J., Couch, F. J., et al. (2008) · Nature · doi:10.1038/nature06633 · Cited by 1,086
A Highly Efficient Recombineering-Based Method for Generating Conditional Knockout Mutations
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Resistance to therapy caused by intragenic deletion in BRCA2
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BRCA2 Is Required for Homology-Directed Repair of Chromosomal Breaks
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Self-citation
Cited by
Causes and consequences of replication stress
Zeman, M. K., & Cimprich, K. A. (2014) · Nature Cell Biology · doi:10.1038/ncb2897 · Cited by 2,079
The multifaceted roles of PARP1 in DNA repair and chromatin remodelling
Ray Chaudhuri, A., & Nussenzweig, A. (2017) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.53 · Cited by 1,786
DNA double-strand break repair-pathway choice in somatic mammalian cells
Scully, R., Panday, A., Elango, R., & Willis, N. A. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0152-0 · Cited by 1,457
Schlacher, K., Wu, H., & Jasin, M. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.05.015 · Cited by 936
Self-citationHomologous Recombination and Human Health: The Roles of BRCA1, BRCA2, and Associated Proteins
Prakash, R., Zhang, Y., Feng, W., & Jasin, M. (2015) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a016600 · Cited by 869
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Metadata
- Authors
- Schlacher, K., Christ, N., Siaud, N., Egashira, A., Wu, H., & Jasin, M.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 145
- Issue
- 4
- Pages
- 529-542
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W1970578083
- Cited by
- 1,255
- References
- 59
- FWCI
- 18.22
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Schlacher, K., Christ, N., Siaud, N., Egashira, A., Wu, H., & Jasin, M. (2011). Double-Strand Break Repair-Independent Role for BRCA2 in Blocking Stalled Replication Fork Degradation by MRE11. Cell. https://doi.org/10.1016/j.cell.2011.03.041
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