Affinage

RAD51D

DNA repair protein RAD51 homolog 4 · UniProt O75771

Length
328 aa
Mass
35.0 kDa
Annotated
2026-04-28
100 papers in source corpus 26 papers cited in narrative 26 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAD51D is a RecA-family ATPase that functions as a core subunit of two distinct heterotetrameric RAD51 paralog complexes — the BCDX2 complex (RAD51B–RAD51C–RAD51D–XRCC2), which promotes nucleation and extension of RAD51 filaments on ssDNA, and the XRCC3 complex (XRCC3–RAD51C–RAD51D–XRCC2), which stably caps RAD51 filament 5′ termini to promote homologous pairing (PMID:37344587, PMID:41196948). RAD51D possesses ssDNA-binding and DNA-stimulated ATPase activities, and its Walker B motif is essential for interaction with XRCC2 and RAD51C and for homologous recombination–mediated repair of DNA double-strand breaks and interstrand crosslinks (PMID:10871607, PMID:16717288, PMID:16236763). RAD51D-deficient cells exhibit profound genomic instability — including elevated mutagenesis, chromosomal rearrangements, telomere attrition and fusions, and extreme sensitivity to PARP inhibitors — establishing RAD51D as essential for error-free DSB repair, telomere maintenance, and suppression of mutagenic alternative repair pathways (PMID:15109494, PMID:16522646, PMID:27924006, PMID:22302683). Germline loss-of-function mutations in RAD51D predispose to ovarian cancer, and somatic reversion mutations restoring RAD51D function confer resistance to PARP inhibitor therapy (PMID:28588062).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2000 High

    Establishing RAD51D as an active ATPase with ssDNA-binding activity that directly heterodimerizes with XRCC2 answered whether RAD51 paralogs possess intrinsic enzymatic function or serve solely as structural scaffolds.

    Evidence Purified recombinant RAD51D protein, in vitro ATPase and DNA-binding assays, co-immunoprecipitation

    PMID:10871607

    Open questions at the time
    • ATPase catalytic cycle parameters not determined
    • stoichiometry of the RAD51D–XRCC2 complex unknown
    • role within higher-order paralog complexes not yet defined
  2. 2000 High

    Demonstrating that Rad51d knockout causes embryonic lethality established RAD51D as essential for cell viability and DNA damage tolerance during replication, setting the stage for p53-rescued cell models.

    Evidence Rad51d-null mouse knockout, embryo phenotyping, MEF culture failure

    PMID:10705376

    Open questions at the time
    • whether lethality reflects replication fork collapse versus accumulated DSBs not distinguished
    • cell-type-specific requirements unknown
  3. 2002 High

    Showing that the purified XRCC2–RAD51D complex catalyzes homologous pairing and forms filamentous structures on ssDNA answered whether this sub-complex has a direct recombinase-like activity.

    Evidence Co-purification from E. coli, in vitro homologous pairing assay, electron microscopy

    PMID:11834724

    Open questions at the time
    • whether this pairing activity is relevant in the context of full RAD51 filaments unknown
    • contribution of individual subunits to pairing not resolved
  4. 2003 High

    Identifying a direct RAD51D–BLM interaction that stimulates Holliday junction disruption linked RAD51 paralog function to recombination intermediate processing.

    Evidence Purified RAD51D–XRCC2 complex, in vitro HJ disruption assay, BLM truncation mutant

    PMID:12975363

    Open questions at the time
    • physiological relevance of RAD51D-stimulated HJ disruption versus dissolution not tested in vivo
    • whether other RAD51 paralogs similarly stimulate BLM unknown
  5. 2004 High

    Demonstrating that RAD51D localizes to telomeres and is required to prevent telomere shortening and end-to-end fusions extended the gene's function beyond DSB repair to telomere protection.

    Evidence Immunofluorescence, ChIP, EM, Rad51d−/− Trp53−/− MEFs, siRNA in ALT cells

    PMID:15109494

    Open questions at the time
    • mechanism of telomeric recruitment unknown
    • whether telomere role is through T-loop HR or shelterin interaction not resolved
  6. 2004 High

    Reconstituting the full BCDX2 heterotetrameric complex and showing it preferentially binds branched DNA and catalyzes strand annealing defined its substrate specificity beyond simple ssDNA binding.

    Evidence Purified BCDX2 complex, competitive DNA-binding with seven substrate types, strand-annealing assay

    PMID:15141025

    Open questions at the time
    • individual subunit contributions to branched DNA recognition not dissected
    • relationship between strand-annealing and RAD51 filament assembly unclear
  7. 2005 High

    Systematic mutagenesis of Walker A and B motifs resolved their distinct roles: Walker A governs ATPase activity and RAD51C interaction, while Walker B is required for XRCC2 and RAD51C binding and HR repair, establishing that RAD51D's ATPase cycle controls complex assembly.

    Evidence Site-directed mutagenesis, complementation in Rad51d-deficient MEFs and CHO cells, yeast two-hybrid, co-IP

    PMID:16236763 PMID:16717288

    Open questions at the time
    • whether ATP hydrolysis by RAD51D is catalytically required or only needed for conformational switching not distinguished
    • structural basis for Walker B–mediated XRCC2 binding unknown at this stage
  8. 2005 High

    Characterizing Rad51d-null MEFs revealed that RAD51D acts upstream of RAD51 focus formation and is required for ICL repair, SCE induction, and suppression of chromosomal instability, placing it mechanistically as a RAD51 mediator.

    Evidence Rad51d−/− Trp53−/− MEFs, RAD51 foci by IF, SCE assay, cytogenetics, DNA damage sensitivity

    PMID:15781618

    Open questions at the time
    • whether RAD51D promotes RAD51 loading or stabilization not distinguished
    • contribution relative to other mediators (BRCA2) not assessed
  9. 2006 High

    Quantifying the mutator phenotype of RAD51D-null cells (12-fold increased mutation rate, elevated gene amplification) established that RAD51D-mediated HR is the primary error-free pathway suppressing diverse classes of genetic instability.

    Evidence Rad51d knockout CHO cells, hprt mutation frequency, dhfr/CAD amplification assays

    PMID:16522646

    Open questions at the time
    • which alternative error-prone pathways are upregulated not fully characterized
    • tissue-specific mutagenic consequences unknown
  10. 2009 Medium

    Mapping the XRCC2-binding interface to the linker region (residues 54–77) and demonstrating that splice variants lacking key domains are non-functional defined the minimal structural requirements for RAD51D activity.

    Evidence Yeast two-hybrid, functional complementation with splice variants in Rad51d-deficient cells

    PMID:19327148

    Open questions at the time
    • structural basis for linker-mediated binding not resolved at atomic level
    • physiological expression levels of splice variants unknown
  11. 2010 High

    Genetic epistasis showing that MLH1 deletion rescues RAD51D-null sensitivity to methylating agents and thiopurines placed RAD51D downstream of MMR-mediated lesion processing, revealing a functional link between mismatch repair and HR.

    Evidence Rad51d−/− Mlh1−/− Trp53−/− triple KO MEFs, MNNG/6-thioG sensitivity, γH2AX, cytogenetics

    PMID:20133210 PMID:21205838

    Open questions at the time
    • whether RAD51D acts at MMR-generated gaps or DSBs not distinguished
    • whether this pathway operates in human cells not confirmed
  12. 2010 High

    Solving the NMR structure of the RAD51D N-terminal domain (four-helix bundle, residues 1–83) and demonstrating its preferential ssDNA binding provided the first atomic-resolution view of a RAD51D functional domain.

    Evidence NMR solution structure, EMSA, NMR titration

    PMID:21111057

    Open questions at the time
    • structure of full-length RAD51D or RAD51D within a complex not available at this time
    • role of N-terminal domain in complex assembly versus DNA engagement not separated
  13. 2010 High

    Identifying SFPQ as a direct RAD51D interactor with synthetic lethal relationship connected RAD51D to RNA-binding protein-mediated genome maintenance.

    Evidence Proteomic co-precipitation, direct interaction assay, synthetic lethality in double-knockdown cells

    PMID:19658102 PMID:20813759

    Open questions at the time
    • molecular basis of synthetic lethality not defined
    • whether SFPQ–RAD51D interaction occurs at DNA damage sites not tested
  14. 2016 High

    Demonstrating that RNF138 ubiquitinates RAD51D to regulate its stability and recruitment to damage sites, while enhancing RAD51D–XRCC2 interaction, revealed a ubiquitin-dependent regulatory layer controlling RAD51D function.

    Evidence Co-IP, ubiquitination assay, RNF138 RING domain mutagenesis, siRNA, RAD51 foci, yeast three-hybrid

    PMID:27161866

    Open questions at the time
    • specific ubiquitin chain type and target lysines on RAD51D not identified
    • whether RNF138 regulation is cell-cycle dependent not tested
  15. 2017 High

    Identifying RAD51D reversion mutations in PARP inhibitor–resistant ovarian cancers and showing that the S207L mutation disrupts XRCC2 binding, HR, and PARPi sensitivity established RAD51D as a clinically actionable HR gene in cancer.

    Evidence Sequencing of matched pre/post-treatment biopsies, patient-derived xenograft, complementation assays, PARPi sensitivity

    PMID:28588062 PMID:28646019

    Open questions at the time
    • frequency of RAD51D-driven PARPi resistance across cancer types not systematically determined
    • whether all RAD51D mutations confer equivalent PARPi sensitivity unknown
  16. 2017 Medium

    Demonstrating that RAD51D loss shifts repair from gene conversion toward SSA and end-joining, causing large chromosomal deletions, mechanistically explained how RAD51D deficiency generates the specific patterns of genomic instability observed in tumors.

    Evidence I-SceI–based HR reporter in isogenic RAD51D-null CHO cells, molecular characterization of repair products

    PMID:27924006

    Open questions at the time
    • whether SSA upregulation is a direct consequence of failed RAD51 loading or secondary effect not determined
    • in vivo relevance in tumor genomes not validated
  17. 2023 High

    Cryo-EM structure of the BCDX2 complex revealed that RAD51C–RAD51D–XRCC2 mimics three RAD51 protomers within a filament, with coupled ATPase activities of RAD51B and RAD51C driving RAD51 nucleation and extension, providing the structural basis for RAD51 paralog-mediated filament assembly.

    Evidence Cryo-EM, AlphaFold2 modeling, single-molecule RAD51 filament assembly assays, ATPase assays

    PMID:37344587

    Open questions at the time
    • role of RAD51D's own ATPase activity within this structural context not fully resolved
    • how BCDX2 is recruited to RPA-coated ssDNA in vivo not defined
  18. 2026 High

    Cryo-EM visualization of RAD51D within two functionally distinct complexes — the RAD51B complex promoting dynamic filament assembly and the XRCC3 complex stably capping filament 5′ ends — unified the field's understanding of how RAD51D participates in both RAD51 nucleation and filament stabilization for homologous pairing.

    Evidence Cryo-EM, biochemical reconstitution

    PMID:41196948

    Open questions at the time
    • how the two complexes coordinate in space and time during repair not resolved
    • whether RAD51D adopts different conformations in the two complexes not fully characterized

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include how RAD51D is recruited to telomeres versus DSB sites, the specific ubiquitin chain linkages and lysine residues mediating RNF138-dependent regulation, and how RAD51D's own ATPase cycle is coordinated with those of RAD51B and RAD51C within the BCDX2 complex.
  • mechanism of telomeric versus DSB-site recruitment unknown
  • RNF138 ubiquitination sites on RAD51D not mapped
  • functional contribution of RAD51D ATPase versus scaffold role within intact complexes not separated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 3 GO:0140657 ATP-dependent activity 3
Localization
GO:0005634 nucleus 2 GO:0005694 chromosome 1
Pathway
R-HSA-73894 DNA Repair 8 R-HSA-1640170 Cell Cycle 2 R-HSA-1643685 Disease 1
Partners
BLMRAD51BRAD51CRNF138SFPQXRCC2XRCC3
Complex memberships
BCDX2 (RAD51B-RAD51C-RAD51D-XRCC2)RAD51D-XRCC2 heterodimerXRCC3 complex (XRCC3-RAD51C-RAD51D-XRCC2)

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 RAD51D (RAD51L3) possesses single-stranded DNA binding activity and DNA-stimulated ATPase activity, and forms a direct heteromeric complex with XRCC2 in human cells, consistent with Walker box motifs in its sequence. Protein purification, in vitro ATPase assay, Co-immunoprecipitation, direct protein-protein interaction with purified proteins The Journal of biological chemistry High 10871607
2002 The purified XRCC2·RAD51D complex catalyzes homologous pairing between single-stranded and double-stranded DNA, and forms ring structures in the absence of DNA and filamentous structures in the presence of ssDNA, similar to RAD51 and XRCC3·RAD51C. Co-expression and purification from E. coli, in vitro homologous pairing assay, electron microscopy The Journal of biological chemistry High 11834724
2003 BLM helicase directly physically associates with RAD51D (RAD51L3) through BLM's N-terminal domain, and the RAD51D-XRCC2 complex stimulates BLM to disrupt synthetic 4-way (Holliday) junctions; this stimulation requires direct BLM-RAD51D contact. Purification of RAD51D-XRCC2 complex, in vitro Holliday junction disruption assay, truncated BLM mutant lacking RAD51D binding, direct physical interaction assay The Journal of biological chemistry High 12975363
2004 RAD51D localizes to telomeres of both meiotic and somatic cells and is required for telomere maintenance; Rad51d-deficient cells show telomeric DNA repeat shortening, elevated chromosomal aberrations including telomeric end-to-end fusions, and siRNA-mediated depletion in telomerase-negative cells also causes telomere erosion and chromosome fusion. Immunofluorescence, electron microscopy, chromatin immunoprecipitation, siRNA knockdown, mouse knockout (Rad51d-/- Trp53-/-) Cell High 15109494
2004 The BCDX2 complex (RAD51B-RAD51C-RAD51D-XRCC2) preferentially binds branched DNA structures (Y-shaped DNA and synthetic Holliday junctions) over linear DNA substrates, and catalyzes strand-annealing between long complementary ssDNA molecules. Competitive DNA-binding assay with seven DNA substrate types, strand-annealing assay with purified complex Nucleic acids research High 15141025
2005 Rad51d-deficient mouse embryonic fibroblasts (rescued by p53 deletion) exhibit sensitivity to interstrand crosslinks, extensive chromosomal instability (aneuploidy, fragments, complex rearrangements), increased centrosome fragmentation, reduced radiation-induced RAD51 focus formation, and failure to induce sister chromatid exchange upon mitomycin C, placing RAD51D upstream of RAD51 focus formation. Rad51d-/- Trp53-/- mouse knockout MEFs, DNA damage sensitivity assays, cytogenetics, immunofluorescence for RAD51 foci, SCE assay Cancer research High 15781618
2006 The Walker B ATPase motif of RAD51D, but not the Walker A motif, is required for interaction with XRCC2 and RAD51C partners and for efficient homologous recombination repair of DNA interstrand crosslinks; B-motif mutants fail to complement rad51d-knockout CHO cells. Site-directed mutagenesis, complementation assay in rad51d KO CHO cells, yeast two- and three-hybrid, co-immunoprecipitation Nucleic acids research High 16717288
2005 Walker Motif A mutations (K113R and K113A) in RAD51D reduce ATP binding/hydrolysis and impair repair of interstrand crosslinks (83-96% reduction); these mutants show ~8-fold reduced interaction with RAD51C while retaining XRCC2 interaction, demonstrating that RAD51D ATPase activity is required for RAD51C binding and HR repair. Site-directed mutagenesis, complementation in Rad51d-deficient MEFs, yeast two-hybrid Mutagenesis High 16236763
2006 RAD51D deficiency (rad51d knockout CHO cells) causes a 12-fold increased rate of hprt mutation and 4-10-fold increased gene amplification, demonstrating that RAD51D-mediated HRR acts in an error-free manner to suppress multiple classes of genetic alterations including chromosomal aberrations and mutagenesis. Rad51d knockout CHO cells, mutation frequency assays (hprt, dhfr, CAD loci), chromosomal aberration analysis Nucleic acids research High 16522646
2010 SFPQ/PSF directly interacts with RAD51D, and deficiency of both proteins confers a synthetic lethal relationship; SFPQ mediates homology-directed DNA repair and DNA damage responses, and SFPQ deficiency alone causes sister chromatid cohesion defects and chromosome instability. Proteomics screen, direct protein interaction assay, synthetic lethality (double knockdown viability), sister chromatid cohesion assay, DNA repair assays Nucleic acids research High 20813759
2010 RAD51D protects cells against MLH1-dependent cytotoxic responses to O6-methylguanine; loss of Mlh1 rescues sensitivity of Rad51d-deficient cells to MNNG (methylating agent), placing RAD51D downstream of MMR in resolving O6-meG-induced recombinogenic lesions. Rad51d-/- Mlh1-/- Trp53-/- triple KO MEFs, MNNG sensitivity assay, gamma-H2AX, G2/M arrest, apoptosis analysis — genetic epistasis DNA repair High 20133210
2010 The N-terminal domain of RAD51D (residues 1-83) has a defined solution structure (four helices flanked by disordered tails), preferentially binds ssDNA over dsDNA via positively charged and hydrophobic surface residues, and this domain mediates XRCC2 interaction; the N-terminal tail is stabilized by hydrophobic interactions (Leu4/Val6 with core residues). NMR solution structure determination, EMSA (DNA binding), NMR titration The international journal of biochemistry & cell biology High 21111057
2011 RAD51D-deficient cells are sensitive to 6-thioguanine; this sensitivity is rescued by Mlh1 deletion, establishing that RAD51D acts downstream of MLH1-mediated MMR processing to resolve recombinogenic 6-thioG lesions. RAD51D deficiency causes chromatid exchange aberrations (triradials/quadriradials) upon 6-thioG treatment. Genetic epistasis (Rad51d-/- Mlh1-/- cells), cytogenetic analysis, drug sensitivity assay Molecular cancer research : MCR High 21205838
2009 From proteomic co-precipitation with purified RAD51D from MEF extracts, SFPQ, NONO, MSH2, and MCM2 were identified as interacting partners of RAD51D; interactions were confirmed by Western blot and ex vivo co-precipitation. Proteomics/mass spectrometry pull-down, Western blot confirmation of interactions Proteomics Medium 19658102
2016 RNF138 E3 ubiquitin ligase directly interacts with RAD51D and ubiquitinates it; RNF138 depletion increases RAD51D protein stability (suggesting ubiquitin-proteasome-mediated degradation), delays RAD51D recruitment to DNA damage sites, reduces RAD51 focus formation and HR efficiency, and sensitizes cells to DNA damage; RNF138 RING domain is required for RAD51D ubiquitination; RNF138 also enhances RAD51D-XRCC2 interaction. Co-immunoprecipitation, ubiquitination assay, RING domain mutagenesis, siRNA depletion, RAD51 focus formation, yeast three-hybrid DNA repair High 27161866
2017 The RAD51D missense mutation p.S207L disrupts the RAD51D-XRCC2 protein-protein interaction, impairs homologous recombination, and confers PARP inhibitor sensitivity, demonstrating that RAD51D-XRCC2 interaction is functionally essential for HR and tumor suppression. In vitro complementation assays, HR assay, PARP inhibitor sensitivity, protein-protein interaction assays Cancer research High 28646019
2019 RAD51D isoform 1 is the functional isoform; isoform 4 (large N-terminal deletion including Walker A) and isoform 6 (alternate N-terminal exon) are non-functional. Cancer-associated mutations G96C and G107V (near/within Walker A) independently disrupt RAD51D-XRCC2 interaction and impair homologous recombination, confirming RAD51D-XRCC2 interaction as essential for DSB repair. Yeast 2- and 3-hybrid, co-immunoprecipitation in U2OS cells, sister chromatid recombination reporter assay in RAD51D KO cells DNA repair High 30836272
2023 Cryo-EM and AlphaFold2 modeling reveal that in the BCDX2 complex, RAD51C-RAD51D-XRCC2 mimics three RAD51 protomers aligned within a nucleoprotein filament, while RAD51B is highly dynamic. BCDX2 stimulates nucleation and extension of RAD51 filaments on ssDNA in reactions dependent on the coupled ATPase activities of RAD51B and RAD51C, orchestrating RAD51 assembly for replication fork protection and DSB repair. Cryo-electron microscopy, AlphaFold2 structural modeling, structural proteomics, biochemical assays, single-molecule analyses, ATPase assays Nature High 37344587
2026 Cryo-EM visualization reveals that RAD51 paralogs form two distinct heterotetrameric complexes: RAD51B-RAD51C-RAD51D-XRCC2 (RAD51B complex) that promotes ATP hydrolysis-dependent dynamic assembly of RAD51 filaments, and XRCC3-RAD51C-RAD51D-XRCC2 (XRCC3 complex) that stably caps the 5' termini of RAD51 filaments to promote homologous pairing. Cryo-electron microscopy, biochemical reconstitution Science (New York, N.Y.) High 41196948
2000 Rad51d-deficient mouse embryos die between 8.5 and 11.5 dpc with generalized developmental defects; embryonic fibroblasts cannot be propagated, establishing that RAD51D is essential for cell viability and normal embryonic development, consistent with a role in repairing DNA damage accumulated during replication. Mouse knockout (gene disruption), embryo phenotyping, MEF culture, gamma radiation/MMS sensitivity of blastocysts Genesis (New York, N.Y. : 2000) High 10705376
2017 Secondary somatic mutations restoring the RAD51D open reading frame were identified in post-progression ovarian carcinoma biopsies from patients treated with the PARP inhibitor rucaparib; in vitro complementation assays and patient-derived xenograft confirmed that these reversion mutations restore HR function and confer PARPi resistance. Sequencing of matched pre/post-treatment biopsies, in vitro complementation assays, patient-derived xenograft Cancer discovery High 28588062
2011 RAD51D-deficient cells are sensitive to PARP inhibitors with >1000-fold sensitivity and show defective RAD51 focus formation in response to PARP inhibitor treatment, confirming RAD51D is required for HR-mediated repair of PARP inhibitor-induced lesions. rad51d null CHO cells, PARP inhibitor sensitivity assay, RAD51 focus formation by immunofluorescence Environmental and molecular mutagenesis Medium 22302683
2022 YTHDF3 promotes RAD51D mRNA translation in an m6A-dependent manner downstream of HNF1α transcriptional upregulation of YTHDF3, establishing a HNF1α/YTHDF3/RAD51D regulatory axis that confers radio-resistance in cervical cancer cells. siRNA knockdown, overexpression, western blot (protein vs. mRNA level), in vitro and in vivo irradiation assays The FEBS journal Medium 36380687
2009 The linker region (residues 54-77) of RAD51D mediates binding to XRCC2; splice variant RAD51DDelta7b (lacking residues 219-223) retains interaction with both RAD51C and XRCC2, while RAD51D+int3 interacts with XRCC2 only; none of the non-full-length splice variants restore mitomycin C resistance in Rad51d-deficient cells. Yeast 2-hybrid, EGFP localization, functional complementation (mitomycin C resistance), RT-PCR expression analysis BMC molecular biology Medium 19327148
2017 RAD51D deficiency shifts DSB repair from homologous recombination-mediated gene conversion toward single-strand annealing (SSA) and end-joining, resulting in large chromosomal deletions at high frequency; RAD51D protects the genome from large deletions by suppressing SSA pathway usage. Loss-of-function HR reporter assay in isogenic CHO cell lines, I-SceI-induced DSBs, molecular characterization of deletion events Nucleic acids research Medium 27924006
2009 The RAD51D E233G variant reduces RAD51C-RAD51D interaction by 2-fold (without affecting XRCC2 interaction), increases cellular resistance to multiple DNA-damaging agents and taxol, reduces anaphase bridge index, and increases proliferation; molecular modeling suggests Glu233 forms a salt bridge with Lys23 in the N-terminal domain that is disrupted by the glycine substitution. Complementation in Rad51d-deficient MEFs, yeast 2-hybrid, anaphase bridge assay, molecular modeling Pharmacogenetics and genomics Medium 19033885

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Germline mutations in RAD51D confer susceptibility to ovarian cancer. Nature genetics 404 21822267
2017 Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma. Cancer discovery 334 28588062
2015 Contribution of Germline Mutations in the RAD51B, RAD51C, and RAD51D Genes to Ovarian Cancer in the Population. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 257 26261251
2004 Telomere maintenance requires the RAD51D recombination/repair protein. Cell 175 15109494
2018 Cost-effectiveness of Population-Based BRCA1, BRCA2, RAD51C, RAD51D, BRIP1, PALB2 Mutation Testing in Unselected General Population Women. Journal of the National Cancer Institute 150 29361001
2000 Midgestation lethality in mice deficient for the RecA-related gene, Rad51d/Rad51l3. Genesis (New York, N.Y. : 2000) 125 10705376
2007 Arabidopsis SNI1 and RAD51D regulate both gene transcription and DNA recombination during the defense response. Proceedings of the National Academy of Sciences of the United States of America 117 17360504
1998 Identification, characterization, and genetic mapping of Rad51d, a new mouse and human RAD51/RecA-related gene. Genomics 108 9570954
2010 The splicing-factor related protein SFPQ/PSF interacts with RAD51D and is necessary for homology-directed repair and sister chromatid cohesion. Nucleic acids research 101 20813759
2000 The RAD51 family member, RAD51L3, is a DNA-stimulated ATPase that forms a complex with XRCC2. The Journal of biological chemistry 92 10871607
2020 BRIP1, RAD51C, and RAD51D mutations are associated with high susceptibility to ovarian cancer: mutation prevalence and precise risk estimates based on a pooled analysis of ~30,000 cases. Journal of ovarian research 83 32359370
2013 Systematic screen identifies miRNAs that target RAD51 and RAD51D to enhance chemosensitivity. Molecular cancer research : MCR 83 24088786
2006 Repression of mutagenesis by Rad51D-mediated homologous recombination. Nucleic acids research 83 16522646
1997 The cytoplasmic DNA-binding protein TraM binds to the inner membrane protein TraD in vitro. Journal of bacteriology 80 9324263
2005 Extensive chromosomal instability in Rad51d-deficient mouse cells. Cancer research 79 15781618
2003 Functional interaction between the Bloom's syndrome helicase and the RAD51 paralog, RAD51L3 (RAD51D). The Journal of biological chemistry 74 12975363
2004 Preferential binding to branched DNA strands and strand-annealing activity of the human Rad51B, Rad51C, Rad51D and Xrcc2 protein complex. Nucleic acids research 72 15141025
2008 Structural basis of specific TraD-TraM recognition during F plasmid-mediated bacterial conjugation. Molecular microbiology 68 18717787
2002 Homologous pairing and ring and filament structure formation activities of the human Xrcc2*Rad51D complex. The Journal of biological chemistry 65 11834724
2022 Moderate penetrance genes complicate genetic testing for breast cancer diagnosis: ATM, CHEK2, BARD1 and RAD51D. Breast (Edinburgh, Scotland) 64 35772246
2004 Thirty-eight C-terminal amino acids of the coupling protein TraD of the F-like conjugative resistance plasmid R1 are required and sufficient to confer binding to the substrate selector protein TraM. Journal of bacteriology 60 15466052
1998 The carboxyl terminus of protein TraD adds specificity and efficiency to F-plasmid conjugative transfer. Journal of bacteriology 58 9811665
2022 Enhancing the BOADICEA cancer risk prediction model to incorporate new data on RAD51C, RAD51D, BARD1 updates to tumour pathology and cancer incidence. Journal of medical genetics 57 36162851
2023 Structure and function of the RAD51B-RAD51C-RAD51D-XRCC2 tumour suppressor. Nature 52 37344587
2006 Disparate requirements for the Walker A and B ATPase motifs of human RAD51D in homologous recombination. Nucleic acids research 51 16717288
2005 Mutations in the C-terminal region of TraM provide evidence for in vivo TraM-TraD interactions during F-plasmid conjugation. Journal of bacteriology 50 15995191
1990 Nucleotide sequence of the promoter-distal region of the tra operon of plasmid R100, including traI (DNA helicase I) and traD genes. Journal of molecular biology 46 2164585
2013 Roles of XRCC2, RAD51B and RAD51D in RAD51-independent SSA recombination. PLoS genetics 45 24278037
2012 A Finnish founder mutation in RAD51D: analysis in breast, ovarian, prostate, and colorectal cancer. Journal of medical genetics 41 22652533
2013 The Arabidopsis RAD51 paralogs RAD51B, RAD51D and XRCC2 play partially redundant roles in somatic DNA repair and gene regulation. The New phytologist 38 24102485
2012 Mutation analysis of RAD51D in non-BRCA1/2 ovarian and breast cancer families. British journal of cancer 37 22415235
1992 Purification and properties of the F sex factor TraD protein, an inner membrane conjugal transfer protein. The Journal of biological chemistry 36 1618779
2022 YTHDF3 mediates HNF1α regulation of cervical cancer radio-resistance by promoting RAD51D translation in an m6A-dependent manner. The FEBS journal 32 36380687
2017 Functionally Null RAD51D Missense Mutation Associates Strongly with Ovarian Carcinoma. Cancer research 31 28646019
2013 Analysis of RAD51D in ovarian cancer patients and families with a history of ovarian or breast cancer. PloS one 31 23372765
2012 Loss of function germline mutations in RAD51D in women with ovarian carcinoma. Gynecologic oncology 31 22986143
1989 Nucleotide sequence of the traD region in the Escherichia coli F sex factor. Gene 30 2680768
2023 Leveraging the microbiome to understand clinical heterogeneity in depression: findings from the T-RAD study. Translational psychiatry 29 37117195
1999 Analysis of F factor TraD membrane topology by use of gene fusions and trypsin-sensitive insertions. Journal of bacteriology 29 10498725
2018 Associations between RAD51D germline mutations and breast cancer risk and survival in BRCA1/2-negative breast cancers. Annals of oncology : official journal of the European Society for Medical Oncology 28 30165555
2005 The ATPase motif in RAD51D is required for resistance to DNA interstrand crosslinking agents and interaction with RAD51C. Mutagenesis 26 16236763
2008 Genome integrity is regulated by the Caenorhabditis elegans Rad51D homolog rfs-1. Genetics 25 18458109
2014 About 1% of the breast and ovarian Spanish families testing negative for BRCA1 and BRCA2 are carriers of RAD51D pathogenic variants. International journal of cancer 23 24130102
2007 TraA, TraC and TraD autorepress two divergent quorum-regulated promoters near the transfer origin of the Ti plasmid of Agrobacterium tumefaciens. Molecular microbiology 23 17367394
2004 Influence of climatic conditions on the mutations in pollen mother cells of Tradescantia clone 4430 and implications for the Trad-MCN bioassay protocol. Hereditas 23 15660975
2004 The variant E233G of the RAD51D gene could be a low-penetrance allele in high-risk breast cancer families without BRCA1/2 mutations. International journal of cancer 22 15170666
2009 The interaction profile of homologous recombination repair proteins RAD51C, RAD51D and XRCC2 as determined by proteomic analysis. Proteomics 21 19658102
2021 A decade of RAD51C and RAD51D germline variants in cancer. Human mutation 20 34923718
2023 Final report of TKI discontinuation trial with dasatinib for the second attempt of treatment-free remission after failing the first attempt with imatinib: Treatment-free Remission Accomplished by Dasatinib (TRAD) study. British journal of haematology 19 37697469
2019 RAD51D splice variants and cancer-associated mutations reveal XRCC2 interaction to be critical for homologous recombination. DNA repair 19 30836272
2016 The recombination mediator RAD51D promotes geminiviral infection. Virology 19 27018825
2009 Genotoxic effects of vehicle traffic pollution as evaluated by micronuclei test in tradescantia (Trad-MCN). Mutation research 19 19386247
2021 Age of ovarian cancer diagnosis among BRIP1, RAD51C, and RAD51D mutation carriers identified through multi-gene panel testing. Journal of ovarian research 18 33926482
1999 Multiple alternative transcripts of the human homologue of the mouse TRAD/R51H3/RAD51D gene, a member of the rec A/RAD51 gene family. Biochemical and biophysical research communications 18 10092526
1998 Regulation of the Enterococcus faecalis pAD1-related sex pheromone response: analyses of traD expression and its role in controlling conjugation functions. Molecular microbiology 18 9791182
1997 Regulation of transfer of the Enterococcus faecalis pheromone-responding plasmid pAD1: temperature-sensitive transfer mutants and identification of a new regulatory determinant, traD. Journal of bacteriology 18 9150221
1996 Construction of derivatives of the F plasmid pOX-tra715: characterization of traY and traD mutants that can be complemented in trans. Molecular microbiology 18 8930905
2016 RNF138 interacts with RAD51D and is required for DNA interstrand crosslink repair and maintaining chromosome integrity. DNA repair 17 27161866
2010 RAD51D protects against MLH1-dependent cytotoxic responses to O(6)-methylguanine. DNA repair 17 20133210
2007 In vivo oligomerization of the F conjugative coupling protein TraD. Journal of bacteriology 17 17631633
2024 Human Fallopian Tube-Derived Organoids with TP53 and RAD51D Mutations Recapitulate an Early Stage High-Grade Serous Ovarian Cancer Phenotype In Vitro. International journal of molecular sciences 16 38255960
2021 RAD51D Aberrant Splicing in Breast Cancer: Identification of Splicing Regulatory Elements and Minigene-Based Evaluation of 53 DNA Variants. Cancers 16 34200360
2017 The homologous recombination protein RAD51D protects the genome from large deletions. Nucleic acids research 16 27924006
2008 Characterization of the traD operon of naphthalene-catabolic plasmid NAH7: a host-range modifier in conjugative transfer. Journal of bacteriology 16 18676671
1989 Transcriptional analysis of the F plasmid surface exclusion region: mapping of traS, traT, and traD transcripts. Plasmid 15 2657819
2018 VirB8 homolog TraE from plasmid pKM101 forms a hexameric ring structure and interacts with the VirB6 homolog TraD. Proceedings of the National Academy of Sciences of the United States of America 14 29784815
2015 Mutation Analysis of the RAD51C and RAD51D Genes in High-Risk Ovarian Cancer Patients and Families from the Czech Republic. PloS one 14 26057125
2013 Hypermethylation of RAD51L3 and XRCC2 genes to predict late toxicity in chemoradiotherapy-treated cervical cancer patients. Folia biologica 14 24485306
1999 Assessment of the genotoxicity of mine-dump material using the Tradescantia-stamen hair (Trad-SHM) and the Tradescantia-micronucleus (Trad-MCN) bioassays. Mutation research 14 10350594
1983 Tradescantia-Micronucleus (Trad-MCN) test on the genotoxicity of malathion. Environmental mutagenesis 14 6861722
2018 Mutational analysis of RAD51C and RAD51D genes in hereditary breast and ovarian cancer families from Murcia (southeastern Spain). European journal of medical genetics 13 29409816
2016 Ubiquitylation of Rad51d Mediated by E3 Ligase Rnf138 Promotes the Homologous Recombination Repair Pathway. PloS one 12 27195665
2012 Uncoupling of RAD51 focus formation and cell survival after replication fork stalling in RAD51D null CHO cells. Environmental and molecular mutagenesis 10 22302683
2023 Arabidopsis lamin-like proteins CRWN1 and CRWN2 interact with SUPPRESSOR OF NPR1-1 INDUCIBLE 1 and RAD51D to prevent DNA damage. The Plant cell 9 37335899
2022 Detection of Orientia tsutsugamushi in Novel Trombiculid Mite Species in Northern Tamil Nadu, India: Use of Targeting the Multicopy traD Gene. Journal of medical entomology 9 34850037
2022 The Genetic and Molecular Analyses of RAD51C and RAD51D Identifies Rare Variants Implicated in Hereditary Ovarian Cancer from a Genetically Unique Population. Cancers 9 35565380
2018 Contribution of RAD51D germline mutations in breast and ovarian cancer in Greece. Journal of human genetics 9 30111881
2011 The homologous recombination protein RAD51D mediates the processing of 6-thioguanine lesions downstream of mismatch repair. Molecular cancer research : MCR 9 21205838
2010 Structural and functional characterization of the N-terminal domain of human Rad51D. The international journal of biochemistry & cell biology 9 21111057
2009 Functional characterization and identification of mouse Rad51d splice variants. BMC molecular biology 9 19327148
2008 Germline mutations in RAD51, RAD51AP1, RAD51B, RAD51C,RAD51D, RAD52 and RAD54L do not contribute to familial chronic lymphocytic leukemia. Leukemia & lymphoma 9 18203022
2019 Association between polymorphisms in MicroRNA target sites of RAD51D genes and risk of hepatocellular carcinoma. Cancer medicine 8 30883040
2009 Functional characterization of the RAD51D E233G genetic variant. Pharmacogenetics and genomics 8 19033885
2009 Cisplatin resistance conferred by the RAD51D (E233G) genetic variant is dependent upon p53 status in human breast carcinoma cell lines. Molecular carcinogenesis 8 19347880
2007 The RAD51D E233G variant and breast cancer risk: population-based and clinic-based family studies of Australian women. Breast cancer research and treatment 8 18058226
2024 Germline testing of BRCA1, BRCA2, PALB2 and CHEK2 c.1100delC in 1514 triple negative familial and isolated breast cancers from a single centre, with extended testing of ATM, RAD51C and RAD51D in over 400. Journal of medical genetics 7 38123987
2023 RAD51D Secondary Mutation-Mediated Resistance to PARP-Inhibitor-Based Therapy in HGSOC. International journal of molecular sciences 7 37833926
2004 Genomic structure and multiple alternative transcripts of the mouse TRAD/RAD51L3/RAD51D gene, a member of the recA/RAD51 gene family. Biochimica et biophysica acta 7 15297144
2023 RAD51C-RAD51D interplays with MSH5 and regulates crossover maturation in rice meiosis. The New phytologist 6 37430391
2022 Clinical characteristics and survival analysis of Chinese ovarian cancer patients with RAD51D germline mutations. BMC cancer 6 36544182
2021 Germline mutations in RAD51C and RAD51D and hereditary predisposition to ovarian cancer. Klinicka onkologie : casopis Ceske a Slovenske onkologicke spolecnosti 5 33657816
2021 New germline mutations in BRCA1, ATM, MUTYH, and RAD51D genes in Tuvans early-onset breast cancer patients. Experimental oncology 4 33785725
2025 Inner membrane components of the plasmid pKM101 type IV secretion system TraE and TraD are DNA-binding proteins. Scientific reports 3 40032854
2022 A phase I/II escalation trial design T-RAD: Treatment of metastatic lung cancer with mRNA-engineered T cells expressing a T cell receptor targeting human telomerase reverse transcriptase (hTERT). Frontiers in oncology 3 36439452
2021 The RAD51D c.82G>A (p.Val28Met) variant disrupts normal splicing and is associated with hereditary ovarian cancer. Breast cancer research and treatment 3 33452952
2002 Mutagenicity of ground water (in the bore-holes) in Ararat Valley (Armenia) detected by Trad-SHM bioassay. Mutation research 3 12113766
2026 Cryo-electron microscopic visualization of RAD51 filament assembly and end-capping by XRCC3-RAD51C-RAD51D-XRCC2. Science (New York, N.Y.) 2 41196948
2022 Serous Tubal Intraepithelial Carcinoma in a Risk-reducing Salpingo-oophorectomy Specimen From a RAD51D Mutation Carrier: A Case Report. International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists 2 35149617
2022 Identification of new RAD51D-regulating microRNAs that also emerge as potent inhibitors of the Fanconi anemia/homologous recombination pathways. Human molecular genetics 2 35904444
1981 Escherichia coli traD(Ts) mutant temperature sensitive for assembly of RNA bacteriophage MS2. Journal of virology 2 7017164