The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection
Open accessAbstract
The appropriate execution of DNA double-strand break (DSB) repair is critical for genome stability and tumor avoidance. 53BP1 and BRCA1 directly influence DSB repair pathway choice by regulating 5' end resection, but how this is achieved remains uncertain. Here we report that Rif1(-/-) mice are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfunctional telomeres. The inappropriate accumulation of RIF1 at DSBs in S phase is antagonized by BRCA1, and deletion of Rif1 suppresses toxic nonhomologous end joining (NHEJ) induced by PARP inhibition in Brca1-deficient cells. Mechanistically, RIF1 is recruited to DSBs via the N-terminal phospho-SQ/TQ domain of 53BP1, and DSBs generated by ionizing radiation or during CSR are hyperresected in the absence of RIF1. Thus, RIF1 and 53BP1 cooperate to block DSB resection to promote NHEJ in G1, which is antagonized by BRCA1 in S phase to ensure a switch of DSB repair mode to homologous recombination.
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Repair Pathway Choices and Consequences at the Double-Strand Break
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DNA double-strand break repair-pathway choice in somatic mammalian cells
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Homologous Recombination Deficiency: Exploiting the Fundamental Vulnerability of Ovarian Cancer
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Replication fork stability confers chemoresistance in BRCA-deficient cells
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Repair of Strand Breaks by Homologous Recombination
Jasin, M., & Rothstein, R. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a012740 · Cited by 887
Metadata
- Authors
- Chapman, J. R., Barral, P., Vannier, J.-B., Borel, V., Steger, M., Tomas-Loba, A., Sartori, A. A., Adams, I. R., Batista, F. D., & Boulton, S. J.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2013-03
- Volume
- 49
- Issue
- 5
- Pages
- 858-871
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2123215808
- Cited by
- 606
- References
- 61
- FWCI
- 28.91
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Chapman, J. R., Barral, P., Vannier, J.-B., Borel, V., Steger, M., Tomas-Loba, A., Sartori, A. A., Adams, I. R., Batista, F. D., & Boulton, S. J. (2013). RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection. Molecular Cell. https://doi.org/10.1016/j.molcel.2013.01.002
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