Relevant bibliographies by topics / RAD51C/XRCC3

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'RAD51C/XRCC3'

Author: Grafiati
Published: 6 September 2023
Last updated: 31 July 2025

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Journal articles on the topic "RAD51C/XRCC3"

1

Somyajit, Kumar, Shivakumar Basavaraju, Ralph Scully, and Ganesh Nagaraju. "ATM- and ATR-Mediated Phosphorylation of XRCC3 Regulates DNA Double-Strand Break-Induced Checkpoint Activation and Repair." Molecular and Cellular Biology 33, no. 9 (2013): 1830–44. http://dx.doi.org/10.1128/mcb.01521-12.

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The RAD51 paralogs XRCC3 and RAD51C have been implicated in homologous recombination (HR) and DNA damage responses. However, the molecular mechanism(s) by which these paralogs regulate HR and DNA damage signaling remains obscure. Here, we show that an SQ motif serine 225 in XRCC3 is phosphorylated by ATR kinase in an ATM signaling pathway. We find that RAD51C but not XRCC2 is essential for XRCC3 phosphorylation, and this modification follows end resection and is specific to S and G 2 phases. XRCC3 phosphorylation is required for chromatin loading of RAD51 and HR-mediated repair of double-stran
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Hatanaka, Atsushi, Mitsuyoshi Yamazoe, Julian E. Sale, et al. "Similar Effects of Brca2 Truncation and Rad51 Paralog Deficiency on Immunoglobulin V Gene Diversification in DT40 Cells Support an Early Role for Rad51 Paralogs in Homologous Recombination." Molecular and Cellular Biology 25, no. 3 (2005): 1124–34. http://dx.doi.org/10.1128/mcb.25.3.1124-1134.2005.

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ABSTRACT BRCA2 is a tumor suppressor gene that is linked to hereditary breast and ovarian cancer. Although the Brca2 protein participates in homologous DNA recombination (HR), its precise role remains unclear. From chicken DT40 cells, we generated BRCA2 gene-deficient cells which harbor a truncation at the 3′ end of the BRC3 repeat (brca2tr). Comparison of the characteristics of brca2tr cells with those of other HR-deficient DT40 clones revealed marked similarities with rad51 paralog mutants (rad51b, rad51c, rad51d, xrcc2, or xrcc3 cells). The phenotypic similarities include a shift from HR-me
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Nagaraju, Ganesh, Andrea Hartlerode, Amy Kwok, Gurushankar Chandramouly, and Ralph Scully. "XRCC2 and XRCC3 Regulate the Balance between Short- and Long-Tract Gene Conversions between Sister Chromatids." Molecular and Cellular Biology 29, no. 15 (2009): 4283–94. http://dx.doi.org/10.1128/mcb.01406-08.

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ABSTRACT Sister chromatid recombination (SCR) is a potentially error-free pathway for the repair of DNA lesions associated with replication and is thought to be important for suppressing genomic instability. The mechanisms regulating the initiation and termination of SCR in mammalian cells are poorly understood. Previous work has implicated all the Rad51 paralogs in the initiation of gene conversion and the Rad51C/XRCC3 complex in its termination. Here, we show that hamster cells deficient in the Rad51 paralog XRCC2, a component of the Rad51B/Rad51C/Rad51D/XRCC2 complex, reveal a bias in favor
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Yamada, Nazumi Alice, John M. Hinz, Vicki L. Kopf, Kathryn D. Segalle, and Larry H. Thompson. "XRCC3 ATPase Activity Is Required for Normal XRCC3-Rad51C Complex Dynamics and Homologous Recombination." Journal of Biological Chemistry 279, no. 22 (2004): 23250–54. http://dx.doi.org/10.1074/jbc.m402247200.

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5

Kurumizaka, H., S. Ikawa, M. Nakada, et al. "Homologous-pairing activity of the human DNA-repair proteins Xrcc3*Rad51C." Proceedings of the National Academy of Sciences 98, no. 10 (2001): 5538–43. http://dx.doi.org/10.1073/pnas.091603098.

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Wiese, C. "Interactions involving the Rad51 paralogs Rad51C and XRCC3 in human cells." Nucleic Acids Research 30, no. 4 (2002): 1001–8. http://dx.doi.org/10.1093/nar/30.4.1001.

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7

Liu, Yilun, Madalena Tarsounas, Paul O'Regan, and Stephen C. West. "Role of RAD51C and XRCC3 in Genetic Recombination and DNA Repair." Journal of Biological Chemistry 282, no. 3 (2006): 1973–79. http://dx.doi.org/10.1074/jbc.m609066200.

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8

Masson, J. Y., A. Z. Stasiak, A. Stasiak, F. E. Benson, and S. C. West. "Complex formation by the human RAD51C and XRCC3 recombination repair proteins." Proceedings of the National Academy of Sciences 98, no. 15 (2001): 8440–46. http://dx.doi.org/10.1073/pnas.111005698.

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Lio, Yi-Ching, David Schild, Mark A. Brenneman, J. Leslie Redpath, and David J. Chen. "Human Rad51C Deficiency Destabilizes XRCC3, Impairs Recombination, and Radiosensitizes S/G2-phase Cells." Journal of Biological Chemistry 279, no. 40 (2004): 42313–20. http://dx.doi.org/10.1074/jbc.m405212200.

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10

Kurumizaka, H. "Region and amino acid residues required for Rad51C binding in the human Xrcc3 protein." Nucleic Acids Research 31, no. 14 (2003): 4041–50. http://dx.doi.org/10.1093/nar/gkg442.

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Dissertations / Theses on the topic "RAD51C/XRCC3"

1

Lu, Daniel Kee. "The Rad51 family of proteins: Interactions, vitamin D, and implications in head and neck cancer." Scholarly Commons, 2013. https://scholarlycommons.pacific.edu/uop_etds/191.

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Protection of the genome from carcinogenic consequences of DNA double-strand breaks (DSBs) is accomplished through the pathways of non-homologous end-joining (NHEJ) or homologous recombinational repair. Five human proteins with homology to Rad51 known as the Rad51 paralogs, Rad51B, Rad51C, Rad51D, XRCC2, and XRCC3, whose loss of function in cell lines leads to high chromosomal instability. Previous studies have shown Rad51C participate in two paralog protein complexes, one containing Rad51B, Rad51C, Rad51D and XRCC2 (BCDX2) and the other containing only Rad51C and XRCC3 (CX3). However, the onl
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2

Mishra, Anup. "Targeting RAD51C Pathological Mutants by Synthetic Lethality and Extended Functions of RAD51C/XRCC3 in Mitochondrial Genome Maintenance." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4155.

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To counteract the potentially calamitous effects of genomic instability in the form of double-strand breaks (DSBs), cells have evolved with two major mechanisms. First, DNA non¬homologous end joining (NHEJ) which requires no significant homology, and second, homologous recombination (HR) that uses intact sequences on the sister chromatid or homologous chromosome as a template to repair the broken DNA. Although NHEJ repairs DSBs in all stages of cell cycle; it is generally error-prone due to insertions or deletions of few nucleotides at the breakpoint. In contrast, DSBs that are generated durin
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