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Journal articles on the topic 'RAD51C/XRCC3'

Author: Grafiati

Published: 6 September 2023

Last updated: 31 July 2025

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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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2

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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3

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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4

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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6

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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9

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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11

Abdu, Uri, Acaimo González-Reyes, Amin Ghabrial, and Trudi Schüpbach. "The Drosophila spn-D Gene Encodes a RAD51C-Like Protein That Is Required Exclusively During Meiosis." Genetics 165, no. 1 (2003): 197–204. http://dx.doi.org/10.1093/genetics/165.1.197.

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Abstract In Drosophila, mutations in double-strand DNA break (DSB) repair enzymes, such as spn-B, activate a meiotic checkpoint leading to dorsal-ventral patterning defects in the egg and an abnormal appearance of the oocyte nucleus. Mutations in spn-D cause an array of ovarian phenotypes similar to spn-B. We have cloned the spn-D locus and found that it encodes a protein of 271 amino acids that shows significant homology to the human RAD51C protein. In mammals the spn-B and spn-D homologs, XRCC3 and RAD51C, play a role in genomic stability in somatic cells. To test for a similar role for spn-

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12

Su, Hang, Zhihao Cheng, Jiyue Huang, et al. "Arabidopsis RAD51, RAD51C and XRCC3 proteins form a complex and facilitate RAD51 localization on chromosomes for meiotic recombination." PLOS Genetics 13, no. 5 (2017): e1006827. http://dx.doi.org/10.1371/journal.pgen.1006827.

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13

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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14

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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15

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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16

Castro, Michael, Ansu Kumar, Himanshu Grover, et al. "Cellworks Omics Biology Model (CBM) to predict therapy response and identify novel biomarkers for 5FU-based combination therapy in gastric cancer patients." Journal of Clinical Oncology 39, no. 15_suppl (2021): e16091-e16091. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e16091.

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e16091 Background: Using a 5FU backbone, a variety of combination chemotherapy regimens have been adopted for gastric cancer. However, the genetic heterogeneity of the disease suggests certain drugs would lead to better outcomes for specific patients. In principle, the incorporation of molecular profiling information into treatment selection can generate superior survival for patients. Therefore, we conducted a pilot study using the CBM to identify novel genomic biomarkers of response and resistance to several 5FU-based regimens. Methods: 12 gastric cancer patients treated with 5FU-cisplatin (

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17

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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18

Kim, So Hyeon, Ahrum Min, Seongyeong Kim, et al. "Abstract LB228: Replication stress activates the DNA damage response and contributes to lapatinib resistance in HER2-positive SK-BR-3 cells." Cancer Research 83, no. 8_Supplement (2023): LB228. http://dx.doi.org/10.1158/1538-7445.am2023-lb228.

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Abstract Background: Lapatinib is a small molecular inhibitor of HER2 and EGFR tyrosine kinases, which is approved for HER2-positive metastatic breast cancer as second line treatment. Significant proportion of patients experience disease progression due to acquired resistance. Activation of DNA damage repair (DDR) is one of the drug-resistance mechanism, however, the impact of DDR on sensitivity to lapatinib is unclear. Thus, lapatinib resistance mechanism was explored from the standpoint of DDR activation. Methods: Acquired lapatinib-resistant (LR) SK-BR-3 cell lines were generated by continu

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19

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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20

Ding, Yan, Can-Lan Sun, Liton Francisco, et al. "Genetic Susceptibility to Therapy-Related Leukemia (t-MDS/AML) After Hodgkin Lymphoma (HL) or Non-Hodgkin Lymphoma (NHL)." Blood 114, no. 22 (2009): 199. http://dx.doi.org/10.1182/blood.v114.22.199.199.

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Abstract Abstract 199 Therapy-induced t-MDS/AML is the leading cause of non-relapse mortality after HL or NHL. However, there exists a wide variation in t-MDS/AML susceptibility – potentially explained by individual variability in drug metabolism, DNA repair and apoptosis, or in genetic profiles shared with de novo AML. Using a matched case-control study design, we examined the association between t-MDS/AML and candidate genes (n=29) in relevant biological pathways, including hematopoietic regulation (RUNX1, HLX1); apoptosis (TP53, MDM2); drug metabolism (CYP3A4, CYP1A1, GSTM1, GSTP1, GSTT1, N

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21

Alolayan, Ashwaq, Fouad Sabatin, Mohammed algarni, et al. "Abstract P6-02-01: Frequency of pathogenic germline mutations beyond Germline BRCA gene mutations among Saudi patients with breast cancer." Cancer Research 83, no. 5_Supplement (2023): P6–02–01—P6–02–01. http://dx.doi.org/10.1158/1538-7445.sabcs22-p6-02-01.

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Abstract Frequency of pathogenic germline mutations beyond Germline BRCA gene mutations among Saudi patients with breast cancer Mohammed Algarni*1,2,3, Ashwaq Alolayan1,2,3, Fouad Sabatin1,2,3, Nadine Mabsout1, Horya Zaher1, Hussam Shehata1, Saeed Alturki4, Abdulaziz alshalhoub1, Fatimah Alturki1, Sadal Refaea1,2,3, Nafisah Abdelhafiz1,2,3, Turki Alfayea 1,2,3, Mohammed Al Balwi1,2,3 Kanan Alshammari1,2,3 1King Abdulaziz Medical City, Ministry of National Guard – Health Affairs, Riyadh, Saudi Arabia, 2King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia, 3King Abdullah

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22

Slupianek, Artur, Shuyue Ren, and Tomasz Skorski. "Selective Anti-Leukemia Targeting of the Interaction Between BCR/ABL and Mammalian RecA Homologs." Blood 112, no. 11 (2008): 195. http://dx.doi.org/10.1182/blood.v112.11.195.195.

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Abstract We showed before that cells transformed by BCR/ABL and other fusion tyrosine kinases (FTKs) such as TEL/ABL, TEL/JAK2 and TEL/PDGFR, inducing chronic myeloproliferative disorders (MPDs), and CD34+ chronic myeloid leukemia (CML) stem/ progenitor cells from chronic phase (CML-CP) and blast crisis (CML-BC) contain an excess of DNA double-strand breaks (DSBs) induced by reactive oxygen species (ROS) and genotoxic stress [Blood, 2005; Cell Cycle, 2006; DNA Repair, 2006; Cancer Res., 2008]. Recent studies also revealed that CD34+CD38− CML-CP and CML-BC stem cellenriched populations seem to

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23

Mpakou, Vassiliki, Evangelia Papadavid, Evi Konsta, et al. "Bortezomib and Methotrexate Interfere with the DNA Repair Signaling Transduction Pathways and Induce Apoptosis in Cutaneous T-Cell Lymphoma." Blood 124, no. 21 (2014): 5232. http://dx.doi.org/10.1182/blood.v124.21.5232.5232.

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Abstract Introduction: Cutaneous T-cell lymphomas (CTCL) represent a heterogeneous group of extranodal non-Hodgkin lymphomas, derived from skin-homing mature T-cells. Mycosis fungoides (MF) and Sézary syndrome (SS) are the commonest types and together comprise 54% of all CTCL. MF evolves from patches to infiltrated plaques and eventually tumors. SS is a lymphoma-leukemia syndrome characterized by erythroderma and the presence of a malignant T-cell clone in the peripheral blood and the skin. At present, no curative treatment for CTCL is available. Therefore current CTCL research efforts are foc

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24

Mishra, Anup, Sneha Saxena, Anjali Kaushal, and Ganesh Nagaraju. "RAD51C/XRCC3 Facilitates Mitochondrial DNA Replication and Maintains Integrity of the Mitochondrial Genome." Molecular and Cellular Biology 38, no. 3 (2017). http://dx.doi.org/10.1128/mcb.00489-17.

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ABSTRACT Mechanisms underlying mitochondrial genome maintenance have recently gained wide attention, as mutations in mitochondrial DNA (mtDNA) lead to inherited muscular and neurological diseases, which are linked to aging and cancer. It was previously reported that human RAD51, RAD51C, and XRCC3 localize to mitochondria upon oxidative stress and are required for the maintenance of mtDNA stability. Since RAD51 and RAD51 paralogs are spontaneously imported into mitochondria, their precise role in mtDNA maintenance under unperturbed conditions remains elusive. Here, we show that RAD51C/XRCC3 is

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25

Szakal, Barnabas, and Dana Branzei. "Hot on RAD51C: structure and functions of RAD51C‐XRCC3." Molecular Oncology, September 8, 2023. http://dx.doi.org/10.1002/1878-0261.13518.

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Abstract: A new study by Longo, Roy et al. has solved the structure of the RAD51C‐XRCC3 (CX3) heterodimer with a bound ATP analog, identifying two main structural interfaces and defining separable replication fork stability roles. One function relates to the ability of RAD51C to bind and assemble CX3 on nascent DNA, with impact on the ability of forks to restart upon replication stress. The other relates to effective CX3 heterodimer formation, required for 5’ RAD51 filament capping, with effects on RAD51 filament disassembly, fork protection and influencing the persistence of reversed forks.

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26

Guh, Chia-Lun, Kai-Hang Lei, Yi-An Chen, et al. "RAD51 paralogs synergize with RAD51 to protect reversed forks from cellular nucleases." Nucleic Acids Research, October 16, 2023. http://dx.doi.org/10.1093/nar/gkad856.

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Abstract Fork reversal is a conserved mechanism to prevent stalled replication forks from collapsing. Formation and protection of reversed forks are two crucial steps in ensuring fork integrity and stability. Five RAD51 paralogs, namely, RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3, which share sequence and structural similarity to the recombinase RAD51, play poorly defined mechanistic roles in these processes. Here, using purified BCDX2 (RAD51BCD-XRCC2) and CX3 (RAD51C-XRCC3) complexes and in vitro reconstituted biochemical systems, we mechanistically dissect their functions in forming and protect

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27

Prakash, Rohit, Yashpal Rawal, Meghan R. Sullivan, et al. "Homologous recombination–deficient mutation cluster in tumor suppressor RAD51C identified by comprehensive analysis of cancer variants." Proceedings of the National Academy of Sciences 119, no. 38 (2022). http://dx.doi.org/10.1073/pnas.2202727119.

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Mutations in homologous recombination (HR) genes, including BRCA1 , BRCA2 , and the RAD51 paralog RAD51C , predispose to tumorigenesis and sensitize cancers to DNA-damaging agents and poly(ADP ribose) polymerase inhibitors. However, ∼800 missense variants of unknown significance have been identified for RAD51C alone, impairing cancer risk assessment and therapeutic strategies. Here, we interrogated >50 RAD51C missense variants, finding that mutations in residues conserved with RAD51 strongly predicted HR deficiency and disrupted interactions with other RAD51 paralogs. A cluster of mutations

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28

Longo, Michael A., Sunetra Roy, Yue Chen, et al. "RAD51C-XRCC3 structure and cancer patient mutations define DNA replication roles." Nature Communications 14, no. 1 (2023). http://dx.doi.org/10.1038/s41467-023-40096-1.

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AbstractRAD51C is an enigmatic predisposition gene for breast, ovarian, and prostate cancer. Currently, missing structural and related functional understanding limits patient mutation interpretation to homology-directed repair (HDR) function analysis. Here we report the RAD51C-XRCC3 (CX3) X-ray co-crystal structure with bound ATP analog and define separable RAD51C replication stability roles informed by its three-dimensional structure, assembly, and unappreciated polymerization motif. Mapping of cancer patient mutations as a functional guide confirms ATP-binding matching RAD51 recombinase, yet

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29

AHLAWAT, SONIKA, REKHA SHARMA, REENA ARORA, et al. "Conserved architecture of RAD51 recombinase in ruminants revealed through molecular cloning and characterization." Indian Journal of Animal Sciences 86, no. 12 (2016). http://dx.doi.org/10.56093/ijans.v86i12.65979.

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Meiotic recombination is a highly conserved process that ensures accurate segregation of homologous chromosomes and contributes to genetic variability of a species to with stand the pressure of natural selection. RAD51 recombinase plays a pivotal role in double strand break repair during homologous recombination and also ensures that chromosomal integrity is maintained during meiotic cell cycle. The present study was aimed to clone and sequence characterize RAD51 gene from cDNA isolated from testicular tissue of four ruminant species (buffalo, cattle, sheep and goat). The complete open reading

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