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1

Tarsounas, Madalena, Adelina A. Davies, and Stephen C. West. "RAD51 localization and activation following DNA damage." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (2004): 87–93. http://dx.doi.org/10.1098/rstb.2003.1368.

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The efficient repair of double–strand breaks in DNA is critical for the maintenance of genome stability. In response to ionizing radiation and other DNA–damaging agents, the RAD51 protein, which is essential for homologous recombination, relocalizes within the nucleus to form distinct foci that can be visualized by microscopy and are thought to represent sites where repair reactions take place. The formation of RAD51 foci in response to DNA damage is dependent upon BRCA2 and a series of proteins known as the RAD51 paralogues (RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3), indicating that the compon
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2

Godin, Stephen K., Meghan R. Sullivan, and Kara A. Bernstein. "Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication." Biochemistry and Cell Biology 94, no. 5 (2016): 407–18. http://dx.doi.org/10.1139/bcb-2016-0012.

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In this review we focus on new insights that challenge our understanding of homologous recombination (HR) and Rad51 regulation. Recent advances using high-resolution microscopy and single molecule techniques have broadened our knowledge of Rad51 filament formation and strand invasion at double-strand break (DSB) sites and at replication forks, which are one of most physiologically relevant forms of HR from yeast to humans. Rad51 filament formation and strand invasion is regulated by many mediator proteins such as the Rad51 paralogues and the Shu complex, consisting of a Shu2/SWS1 family member
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3

Liu, Jie, Ludovic Renault, Xavier Veaute, Francis Fabre, Henning Stahlberg, and Wolf-Dietrich Heyer. "Rad51 paralogues Rad55–Rad57 balance the antirecombinase Srs2 in Rad51 filament formation." Nature 479, no. 7372 (2011): 245–48. http://dx.doi.org/10.1038/nature10522.

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4

Angelis, Karel J., Lenka Záveská Drábková, Radka Vágnerová, and Marcela Holá. "RAD51 and RAD51B Play Diverse Roles in the Repair of DNA Double Strand Breaks in Physcomitrium patens." Genes 14, no. 2 (2023): 305. http://dx.doi.org/10.3390/genes14020305.

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RAD51 is involved in finding and invading homologous DNA sequences for accurate homologous recombination (HR). Its paralogs have evolved to regulate and promote RAD51 functions. The efficient gene targeting and high HR rates are unique in plants only in the moss Physcomitrium patens (P. patens). In addition to two functionally equivalent RAD51 genes (RAD1-1 and RAD51-2), other RAD51 paralogues were also identified in P. patens. For elucidation of RAD51’s involvement during DSB repair, two knockout lines were constructed, one mutated in both RAD51 genes (Pprad51-1-2) and the second with mutated
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5

Khoo, Kelvin H. P., Hayley R. Jolly, and Jason A. Able. "The RAD51 gene family in bread wheat is highly conserved across eukaryotes, with RAD51A upregulated during early meiosis." Functional Plant Biology 35, no. 12 (2008): 1267. http://dx.doi.org/10.1071/fp08203.

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The RADiation sensitive protein 51 (RAD51) recombinase is a eukaryotic homologue of the bacterial Recombinase A (RecA). It is required for homologous recombination of DNA during meiosis where it plays a role in processes such as homology searching and strand invasion. RAD51 is well conserved in eukaryotes with as many as four paralogues identified in vertebrates and some higher plants. Here we report the isolation and preliminary characterisation of four RAD51 gene family members in hexaploid (bread) wheat (Triticum aestivum L.). RAD51A1, RAD51A2 and RAD51D were located on chromosome group 7,
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6

Pohl, Thomas J., and Jac A. Nickoloff. "Rad51-Independent Interchromosomal Double-Strand Break Repair by Gene Conversion Requires Rad52 but Not Rad55, Rad57, or Dmc1." Molecular and Cellular Biology 28, no. 3 (2007): 897–906. http://dx.doi.org/10.1128/mcb.00524-07.

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ABSTRACT Homologous recombination (HR) is critical for DNA double-strand break (DSB) repair and genome stabilization. In yeast, HR is catalyzed by the Rad51 strand transferase and its “mediators,” including the Rad52 single-strand DNA-annealing protein, two Rad51 paralogs (Rad55 and Rad57), and Rad54. A Rad51 homolog, Dmc1, is important for meiotic HR. In wild-type cells, most DSB repair results in gene conversion, a conservative HR outcome. Because Rad51 plays a central role in the homology search and strand invasion steps, DSBs either are not repaired or are repaired by nonconservative singl
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7

Badie, Sophie, Chunyan Liao, Maria Thanasoula, Paul Barber, Mark A. Hill, and Madalena Tarsounas. "RAD51C facilitates checkpoint signaling by promoting CHK2 phosphorylation." Journal of Cell Biology 185, no. 4 (2009): 587–600. http://dx.doi.org/10.1083/jcb.200811079.

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The RAD51 paralogues act in the homologous recombination (HR) pathway of DNA repair. Human RAD51C (hRAD51C) participates in branch migration and Holliday junction resolution and thus is important for processing HR intermediates late in the DNA repair process. Evidence for early involvement of RAD51 during DNA repair also exists, but its function in this context is not understood. In this study, we demonstrate that RAD51C accumulates at DNA damage sites concomitantly with the RAD51 recombinase and is retained after RAD51 disassembly, which is consistent with both an early and a late function fo
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8

Godin, Stephen, Adam Wier, Faiz Kabbinavar, et al. "The Shu complex interacts with Rad51 through the Rad51 paralogues Rad55–Rad57 to mediate error-free recombination." Nucleic Acids Research 41, no. 8 (2013): 4525–34. http://dx.doi.org/10.1093/nar/gkt138.

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9

Yang, Yongjia, Jihong Guo, Lei Dai, et al. "XRCC2 mutation causes meiotic arrest, azoospermia and infertility." Journal of Medical Genetics 55, no. 9 (2018): 628–36. http://dx.doi.org/10.1136/jmedgenet-2017-105145.

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BackgroundMeiotic homologous recombination (HR) plays an essential role in gametogenesis. In most eukaryotes, meiotic HR is mediated by two recombinase systems: ubiquitous RAD51 and meiosis-specific DMC1. In the RAD51-mediated HR system, RAD51 and five RAD51 paralogues are essential for normal RAD51 function, but the role of RAD51 in human meiosis is unclear. The knockout of Rad51 or any Rad51 paralogue in mice exhibits embryonic lethality. We investigated a family with meiotic arrest, azoospermia and infertility but without other abnormalities.MethodsHomozygosity mapping and whole-exome seque
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10

Roy, Upasana, and Eric C. Greene. "The Role of the Rad55–Rad57 Complex in DNA Repair." Genes 12, no. 9 (2021): 1390. http://dx.doi.org/10.3390/genes12091390.

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Homologous recombination (HR) is a mechanism conserved from bacteria to humans essential for the accurate repair of DNA double-stranded breaks, and maintenance of genome integrity. In eukaryotes, the key DNA transactions in HR are catalyzed by the Rad51 recombinase, assisted by a host of regulatory factors including mediators such as Rad52 and Rad51 paralogs. Rad51 paralogs play a crucial role in regulating proper levels of HR, and mutations in the human counterparts have been associated with diseases such as cancer and Fanconi Anemia. In this review, we focus on the Saccharomyces cerevisiae R
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11

Tsukamoto, Mariko, Kentaro Yamashita, Toshiko Miyazaki, Miki Shinohara, and Akira Shinohara. "The N-Terminal DNA-Binding Domain of Rad52 PromotesRAD51-Independent Recombination inSaccharomyces cerevisiae." Genetics 165, no. 4 (2003): 1703–15. http://dx.doi.org/10.1093/genetics/165.4.1703.

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AbstractIn Saccharomyces cerevisiae, the Rad52 protein plays a role in both RAD51-dependent and RAD51-independent recombination pathways. We characterized a rad52 mutant, rad52-329, which lacks the C-terminal Rad51-interacting domain, and studied its role in RAD51-independent recombination. The rad52-329 mutant is completely defective in mating-type switching, but partially proficient in recombination between inverted repeats. We also analyzed the effect of the rad52-329 mutant on telomere recombination. Yeast cells lacking telomerase maintain telomere length by recombination. The rad52-329 mu
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12

Sullivan, Meghan R., and Kara A. Bernstein. "RAD-ical New Insights into RAD51 Regulation." Genes 9, no. 12 (2018): 629. http://dx.doi.org/10.3390/genes9120629.

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The accurate repair of DNA is critical for genome stability and cancer prevention. DNA double-strand breaks are one of the most toxic lesions; however, they can be repaired using homologous recombination. Homologous recombination is a high-fidelity DNA repair pathway that uses a homologous template for repair. One central HR step is RAD51 nucleoprotein filament formation on the single-stranded DNA ends, which is a step required for the homology search and strand invasion steps of HR. RAD51 filament formation is tightly controlled by many positive and negative regulators, which are collectively
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13

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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14

Bernstein, Kara A., Robert J. D. Reid, Ivana Sunjevaric, Kimberly Demuth, Rebecca C. Burgess, and Rodney Rothstein. "The Shu complex, which contains Rad51 paralogues, promotes DNA repair through inhibition of the Srs2 anti-recombinase." Molecular Biology of the Cell 22, no. 9 (2011): 1599–607. http://dx.doi.org/10.1091/mbc.e10-08-0691.

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The Shu complex, which contains RAD51 paralogues, is involved in the decision between homologous recombination and error-prone repair. We discovered a link to ribosomal DNA (rDNA) recombination when we found an interaction between one member of the Shu complex, SHU1, and UAF30, a component of the upstream activating factor complex (UAF), which regulates rDNA transcription. In the absence of Uaf30, rDNA copy number increases, and this increase depends on several functional subunits of the Shu complex. Furthermore, in the absence of Uaf30, we find that Shu1 and Srs2, an anti-recombinase DNA heli
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15

Dobson, Rachel, Christopher Stockdale, Craig Lapsley, Jonathan Wilkes, and Richard McCulloch. "Interactions among Trypanosoma brucei RAD51 paralogues in DNA repair and antigenic variation." Molecular Microbiology 81, no. 2 (2011): 434–56. http://dx.doi.org/10.1111/j.1365-2958.2011.07703.x.

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16

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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17

Simo Cheyou, Estelle, Jacopo Boni, Jonathan Boulais, et al. "Systematic proximal mapping of the classical RAD51 paralogs unravel functionally and clinically relevant interactors for genome stability." PLOS Genetics 18, no. 11 (2022): e1010495. http://dx.doi.org/10.1371/journal.pgen.1010495.

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Homologous recombination (HR) plays an essential role in the maintenance of genome stability by promoting the repair of cytotoxic DNA double strand breaks (DSBs). More recently, the HR pathway has emerged as a core component of the response to replication stress, in part by protecting stalled replication forks from nucleolytic degradation. In that regard, the mammalian RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3) have been involved in both HR-mediated DNA repair and collapsed replication fork resolution. Still, it remains largely obscure how they participate in both processes, the
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18

Maloisel, Laurent, Emilie Ma, Jamie Phipps, et al. "Rad51 filaments assembled in the absence of the complex formed by the Rad51 paralogs Rad55 and Rad57 are outcompeted by translesion DNA polymerases on UV-induced ssDNA gaps." PLOS Genetics 19, no. 2 (2023): e1010639. http://dx.doi.org/10.1371/journal.pgen.1010639.

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The bypass of DNA lesions that block replicative polymerases during DNA replication relies on DNA damage tolerance pathways. The error-prone translesion synthesis (TLS) pathway depends on specialized DNA polymerases that incorporate nucleotides in front of base lesions, potentially inducing mutagenesis. Two error-free pathways can bypass the lesions: the template switching pathway, which uses the sister chromatid as a template, and the homologous recombination pathway (HR), which also can use the homologous chromosome as template. The balance between error-prone and error-free pathways control
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19

Arakawa, Hiroshi, and Jean-Marie Buerstedde. "Activation-induced cytidine deaminase-mediated hypermutation in the DT40 cell line." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1517 (2008): 639–44. http://dx.doi.org/10.1098/rstb.2008.0202.

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Depending on the species and the developmental stage of B cells, activation-induced cytidine deaminase (AID) triggers immunoglobulin ( Ig ) gene diversification by gene conversion, hypermutation or switch recombination. The bursal B cell line DT40 usually diversifies its rearranged Ig light chain ( IgL ) gene by gene conversion, but disruption of the RAD51 gene paralogues or deletion of the ψV conversion donors induces hypermutation. Although not all aspects of somatic hypermutation can be studied in DT40, the compact size of the chicken IgL locus and the ability to modify the genome by target
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20

Daboussi, Fayza, John Thacker, and Bernard S. Lopez. "Genetic interactions between RAD51 and its paralogues for centrosome fragmentation and ploidy control, independently of the sensitivity to genotoxic stresses." Oncogene 24, no. 22 (2005): 3691–96. http://dx.doi.org/10.1038/sj.onc.1208438.

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21

Wesoly, Joanna, Sheba Agarwal, Stefan Sigurdsson, et al. "Differential Contributions of Mammalian Rad54 Paralogs to Recombination, DNA Damage Repair, and Meiosis." Molecular and Cellular Biology 26, no. 3 (2006): 976–89. http://dx.doi.org/10.1128/mcb.26.3.976-989.2006.

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ABSTRACT Homologous recombination is a versatile DNA damage repair pathway requiring Rad51 and Rad54. Here we show that a mammalian Rad54 paralog, Rad54B, displays physical and functional interactions with Rad51 and DNA that are similar to those of Rad54. While ablation of Rad54 in mouse embryonic stem (ES) cells leads to a mild reduction in homologous recombination efficiency, the absence of Rad54B has little effect. However, the absence of both Rad54 and Rad54B dramatically reduces homologous recombination efficiency. Furthermore, we show that Rad54B protects ES cells from ionizing radiation
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22

Takata, Minoru, Masao S. Sasaki, Eiichiro Sonoda, et al. "The Rad51 Paralog Rad51B Promotes Homologous Recombinational Repair." Molecular and Cellular Biology 20, no. 17 (2000): 6476–82. http://dx.doi.org/10.1128/mcb.20.17.6476-6482.2000.

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ABSTRACT The highly conserved Saccharomyces cerevisiae Rad51 protein plays a central role in both mitotic and meiotic homologous DNA recombination. Seven members of the Rad51 family have been identified in vertebrate cells, including Rad51, Dmc1, and five Rad51-related proteins referred to as Rad51 paralogs, which share 20 to 30% sequence identity with Rad51. In chicken B lymphocyte DT40 cells, we generated a mutant with RAD51B/RAD51L1, a member of the Rad51 family, knocked out. RAD51B −/− cells are viable, although spontaneous chromosomal aberrations kill about 20% of the cells in each cell c
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23

Sinha, Asha, Ali Saleh, Raelene Endersby, et al. "RAD51-Mediated DNA Homologous Recombination Is Independent of PTEN Mutational Status." Cancers 12, no. 11 (2020): 3178. http://dx.doi.org/10.3390/cancers12113178.

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PTEN mutation occurs in a variety of aggressive cancers and is associated with poor patient outcomes. Recent studies have linked mutational loss of PTEN to reduced RAD51 expression and function, a key factor involved in the homologous recombination (HR) pathway. However, these studies remain controversial, as they fail to establish a definitive causal link to RAD51 expression that is PTEN-dependent, while other studies have not been able to recapitulate the relationship between the PTEN expression and the RAD51/HR function. Resolution of this apparent conundrum is essential due to the clinical
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24

Takata, Minoru, Masao S. Sasaki, Seiji Tachiiri, et al. "Chromosome Instability and Defective Recombinational Repair in Knockout Mutants of the Five Rad51 Paralogs." Molecular and Cellular Biology 21, no. 8 (2001): 2858–66. http://dx.doi.org/10.1128/mcb.21.8.2858-2866.2001.

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ABSTRACT The Rad51 protein, a eukaryotic homologue of Escherichia coli RecA, plays a central role in both mitotic and meiotic homologous DNA recombination (HR) in Saccharomyces cerevisiae and is essential for the proliferation of vertebrate cells. Five vertebrate genes, RAD51B, -C, and -D and XRCC2 and -3, are implicated in HR on the basis of their sequence similarity to Rad51 (Rad51 paralogs). We generated mutants deficient in each of these proteins in the chicken B-lymphocyte DT40 cell line and report here the comparison of four new mutants and their complemented derivatives with our previou
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25

van Veelen, Lieneke R., Jeroen Essers, Mandy W. M. M. van de Rakt, et al. "Ionizing radiation-induced foci formation of mammalian Rad51 and Rad54 depends on the Rad51 paralogs, but not on Rad52." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 574, no. 1-2 (2005): 34–49. http://dx.doi.org/10.1016/j.mrfmmm.2005.01.020.

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26

Alagpulinsa, David, Srinivas Ayyadevara, Shmuel Yaccoby, and Robert shmookler Reis. "A Peptide Nucleic Acid Targeting Nuclear Rad51 Sensitizes Myeloma Cells to Melphalan Chemotoxicity Both in Vitro and in Vivo." Blood 124, no. 21 (2014): 3529. http://dx.doi.org/10.1182/blood.v124.21.3529.3529.

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Abstract Multiple myeloma (MM) cells are characterized by extensive genomic heterogeneity, which contributes to patient differences in prognosis and response to treatment. We previously reported that MM cells have elevated homologous recombination (HR) rates and expression of RAD51 and its paralogs, promoting genomic instability and disease progression that are reversed by RAD51 siRNA. We now examine the roles of HR and RAD51 in resistance to melphalan, one of the most widely used drugs for MM chemotherapy. The drug induces a variety of DNA lesions, with DNA interstrand crosslinks (ICL) accoun
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27

Darrah, Kristie, Katherine Oppenheimer, Nicole Banks, et al. "Abstract 1466: Comprehensive analysis of breast and ovarian cancer-identified RAD51D variants." Cancer Research 85, no. 8_Supplement_1 (2025): 1466. https://doi.org/10.1158/1538-7445.am2025-1466.

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Abstract The RAD51 paralogs are essential genes in coordinating the early steps of homologous recombination (HR)-mediated repair of DNA double strand breaks (DSBs). Currently, there are over 300 epidemiology studies linking a single mutation or polymorphism in one of the five canonical RAD51 paralogs to cancer predisposition and tumorigenesis. As one of the most frequently mutated RAD51 paralogs, mutations in RAD51D have been identified in 5% of hereditary ovarian cancers and pathogenic variants are associated with a 25% lifetime risk for breast cancer. We have uncovered more than 160 patient-
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28

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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29

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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30

Mohamed, Ruzianisra. "Homology Modeling of Human DNA Repair Protein RAD51 Homolog 3 (RAD51C) in Breast Cancer." International Journal of Pharmaceuticals, Nutraceuticals and Cosmetic Science 7, no. 2 (2024): 136–49. https://doi.org/10.24191/ijpnacs.v7i2.11.

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Breast cancer is known as one of the most predominant cancers that affect both females and males worldwide. The most crucial risk factor in breast cancer is the mutations in the RAD51C gene that have been considered in most hereditary breast cancers. RAD51C, the RAD51 paralogs, is also a deoxyribonucleic acid (DNA) repair protein related to breast and ovarian cancers. DNA double-strand breaks (DSBs) account for the significant detrimental form of DNA damage. RAD51C mutants also have been recognized in breast/ovarian cancer patients. However, the role of the RAD51C protein in hereditary breast
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31

Liu, N. "Involvement of Rad51C in two distinct protein complexes of Rad51 paralogs in human cells." Nucleic Acids Research 30, no. 4 (2002): 1009–15. http://dx.doi.org/10.1093/nar/30.4.1009.

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32

Bonilla, Braulio, Sarah R. Hengel, McKenzie K. Grundy, and Kara A. Bernstein. "RAD51 Gene Family Structure and Function." Annual Review of Genetics 54, no. 1 (2020): 25–46. http://dx.doi.org/10.1146/annurev-genet-021920-092410.

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Accurate DNA repair and replication are critical for genomic stability and cancer prevention. RAD51 and its gene family are key regulators of DNA fidelity through diverse roles in double-strand break repair, replication stress, and meiosis. RAD51 is an ATPase that forms a nucleoprotein filament on single-stranded DNA. RAD51 has the function of finding and invading homologous DNA sequences to enable accurate and timely DNA repair. Its paralogs, which arose from ancient gene duplications of RAD51, have evolved to regulate and promote RAD51 function. Underscoring its importance, misregulation of
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33

Sullivan, Katherine, Kimberly Cramer-Morales, Daniel L. McElroy, et al. "Identification of a Small Molecule Inhibitor of RAD52 to Induce Synthetic Lethality in BRCA-Deficient Leukemias." Blood 126, no. 23 (2015): 4434. http://dx.doi.org/10.1182/blood.v126.23.4434.4434.

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Abstract Altered DNA repair mechanisms are responsible for survival of leukemia stem cells (LSCs) and/or leukemia progenitor cells (LPCs) accumulating numerous lethal DNA double-strand breaks (DSBs). DSBs resulting from stalled/broken replication forks in proliferating cells are primarily repaired by RAD51-mediated homologous recombination repair (HR), which depends on BRCA1-PALB2-BRCA2-RAD51 paralogs (BRCA pathway), while RAD52 pathway serves as redundant back-up mechanism. Enhanced self-renewal of LSCs and high proliferation rate of LPCs commit them to HR. It has been reported that inhibitio
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34

Taylor, Martin R. G., Mário Špírek, Kathy R. Chaurasiya, et al. "Rad51 Paralogs Remodel Pre-synaptic Rad51 Filaments to Stimulate Homologous Recombination." Cell 162, no. 2 (2015): 271–86. http://dx.doi.org/10.1016/j.cell.2015.06.015.

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35

Taylor, Martin R. G., Mário Špírek, Chu Jian Ma, et al. "A Polar and Nucleotide-Dependent Mechanism of Action for RAD51 Paralogs in RAD51 Filament Remodeling." Molecular Cell 64, no. 5 (2016): 926–39. http://dx.doi.org/10.1016/j.molcel.2016.10.020.

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36

Cejka, Petr. "Single-molecule studies illuminate the function of RAD51 paralogs." Molecular Cell 81, no. 5 (2021): 898–900. http://dx.doi.org/10.1016/j.molcel.2021.01.037.

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37

Schild, David, Yi-ching Lio, David W. Collins, Tswakai Tsomondo, and David J. Chen. "Evidence for Simultaneous Protein Interactions between Human Rad51 Paralogs." Journal of Biological Chemistry 275, no. 22 (2000): 16443–49. http://dx.doi.org/10.1074/jbc.m001473200.

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38

Bhattacharya, Debanjali, Satyaranjan Sahoo, Tarun Nagraj, Suruchi Dixit, Harsh Kumar Dwivedi, and Ganesh Nagaraju. "RAD51 paralogs: Expanding roles in replication stress responses and repair." Current Opinion in Pharmacology 67 (December 2022): 102313. http://dx.doi.org/10.1016/j.coph.2022.102313.

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39

Adelman, Carrie A., Rafal L. Lolo, Nicolai J. Birkbak, et al. "HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis." Nature 502, no. 7471 (2013): 381–84. http://dx.doi.org/10.1038/nature12565.

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40

Anand, Roopesh, Erika Buechelmaier, Ondrej Belan, et al. "HELQ is a dual-function DSB repair enzyme modulated by RPA and RAD51." Nature 601, no. 7892 (2021): 268–73. http://dx.doi.org/10.1038/s41586-021-04261-0.

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AbstractDNA double-stranded breaks (DSBs) are deleterious lesions, and their incorrect repair can drive cancer development1. HELQ is a superfamily 2 helicase with 3′ to 5′ polarity, and its disruption in mice confers germ cells loss, infertility and increased predisposition to ovarian and pituitary tumours2–4. At the cellular level, defects in HELQ result in hypersensitivity to cisplatin and mitomycin C, and persistence of RAD51 foci after DNA damage3,5. Notably, HELQ binds to RPA and the RAD51-paralogue BCDX2 complex, but the relevance of these interactions and how HELQ functions in DSB repai
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Rodrigue, Amélie, Yan Coulombe, Karine Jacquet, et al. "The RAD51 paralogs ensure cellular protection against mitotic defects and aneuploidy." Journal of Cell Science 126, no. 1 (2012): 348–59. http://dx.doi.org/10.1242/jcs.114595.

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Genois, Marie-Michelle, Marie Plourde, Chantal Éthier, et al. "Roles of Rad51 paralogs for promoting homologous recombination in Leishmania infantum." Nucleic Acids Research 43, no. 5 (2015): 2701–15. http://dx.doi.org/10.1093/nar/gkv118.

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Suwaki, Natsuko, Kerstin Klare, and Madalena Tarsounas. "RAD51 paralogs: Roles in DNA damage signalling, recombinational repair and tumorigenesis." Seminars in Cell & Developmental Biology 22, no. 8 (2011): 898–905. http://dx.doi.org/10.1016/j.semcdb.2011.07.019.

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Ordinario, Ellen C., Munehisa Yabuki, Priya Handa, W. Jason Cummings, and Nancy Maizels. "RAD51 paralogs promote homology-directed repair at diversifying immunoglobulin V regions." BMC Molecular Biology 10, no. 1 (2009): 98. http://dx.doi.org/10.1186/1471-2199-10-98.

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Masson, J. Y. "Identification and purification of two distinct complexes containing the five RAD51 paralogs." Genes & Development 15, no. 24 (2001): 3296–307. http://dx.doi.org/10.1101/gad.947001.

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Jensen, Ryan B., Ali Ozes, Taeho Kim, Allison Estep, and Stephen C. Kowalczykowski. "BRCA2 is epistatic to the RAD51 paralogs in response to DNA damage." DNA Repair 12, no. 4 (2013): 306–11. http://dx.doi.org/10.1016/j.dnarep.2012.12.007.

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Bleuyard, Jean-Yves, Maria E. Gallego, Florence Savigny, and Charles I. White. "Differing requirements for the Arabidopsis Rad51 paralogs in meiosis and DNA repair." Plant Journal 41, no. 4 (2004): 533–45. http://dx.doi.org/10.1111/j.1365-313x.2004.02318.x.

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Somyajit, Kumar, Sneha Saxena, Sharath Babu, Anup Mishra, and Ganesh Nagaraju. "Mammalian RAD51 paralogs protect nascent DNA at stalled forks and mediate replication restart." Nucleic Acids Research 48, no. 9 (2020): 5196–97. http://dx.doi.org/10.1093/nar/gkaa279.

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Xu, Zhan, Jianxiang Zhang, Meng Xu, et al. "Rice RAD51 paralogs play essential roles in somatic homologous recombination for DNA repair." Plant Journal 95, no. 2 (2018): 282–95. http://dx.doi.org/10.1111/tpj.13949.

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Harris, Janelle Louise, Andrea Rabellino, and Kum Kum Khanna. "RAD51 paralogs promote genomic integrity and chemoresistance in cancer by facilitating homologous recombination." Annals of Translational Medicine 6, S2 (2018): S122. http://dx.doi.org/10.21037/atm.2018.12.30.

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