Affinage

RAD51C

DNA repair protein RAD51 homolog 3 · UniProt O43502

Length
376 aa
Mass
42.2 kDa
Annotated
2026-06-10
100 papers in source corpus 42 papers cited in narrative 42 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAD51C is a central RAD51 paralog that organizes homologous recombination (HR) by serving as the shared, catalytic hub of two distinct paralog complexes—BCDX2 (RAD51B–RAD51C–RAD51D–XRCC2) and CX3 (RAD51C–XRCC3)—and is required for assembly of both (PMID:11744692, PMID:11842113, PMID:11912211). RAD51C contributes ssDNA-binding, DNA-stimulated ATPase, and homologous-pairing/strand-annealing activities to these complexes, and acts as a recombination mediator that relieves RPA inhibition to promote RAD51 loading (PMID:11331762, PMID:11751636, PMID:15141025). Cryo-EM and X-ray structures show that within BCDX2 the RAD51C–RAD51D–XRCC2 module mimics three RAD51 protomers to nucleate and extend RAD51 filaments on ssDNA in a manner dependent on the coupled ATPase activities of RAD51B and RAD51C, while CX3 binds ATP like RAD51 and contributes a polymerization/5′-capping motif governing replication fork protection, restart, and reversal (PMID:37344587, PMID:37488098). Functionally, RAD51C is required for DNA-damage-induced RAD51 focus formation, Holliday-junction branch migration and resolution, and BRCA2-independent nuclear import of RAD51, and it also acts upstream in damage signaling by enabling ATM/NBS1/RPA-dependent recruitment and CHK2-dependent checkpoint activation (PMID:12000837, PMID:14716019, PMID:19451272, PMID:19783859). Beyond canonical HR it joins a PALB2–BRCA2 complex, localizes to mitochondrial nucleoids with XRCC3 to support mtDNA maintenance, and stimulates ALKBH3-mediated demethylation repair (PMID:24141787, PMID:29158291, PMID:31642493). RAD51C is a tumor suppressor: biallelic mutation causes a Fanconi anemia–like disorder (FANCO) and monoallelic loss-of-function confers breast and ovarian cancer susceptibility with PARP-inhibitor sensitivity, while reversion mutations and loss of promoter methylation drive PARPi resistance (PMID:20400963, PMID:28588062, PMID:34321239).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1998 Medium

    Establishing RAD51C as a RAD51-family member that binds other paralogs rather than self answered whether it acts as a mediator/accessory factor rather than the core recombinase.

    Evidence cDNA cloning and yeast two-hybrid interaction mapping with XRCC3 and RAD51B

    PMID:9469824

    Open questions at the time
    • Interactions not validated biochemically with purified proteins
    • No functional or DNA-binding activity demonstrated
  2. 2001 High

    Reconstitution of stable RAD51C–XRCC3 and RAD51B–RAD51C complexes with DNA-binding, ATPase, pairing and mediator activities defined RAD51C as the catalytic subunit that facilitates RAD51-driven strand exchange.

    Evidence Baculovirus co-expression, co-purification, endogenous Co-IP, in vitro homologous-pairing and strand-exchange assays, ATPase assays, electron microscopy

    PMID:11331762 PMID:11459987 PMID:11744692 PMID:11751636

    Open questions at the time
    • Stoichiometry and architecture of complexes not resolved
    • How mediator activity relates to in vivo RAD51 loading unclear
  3. 2002 High

    Mapping RAD51C into two mutually exclusive in vivo complexes (BCDX2 and CX3) with RAD51C as the obligate shared subunit established the paralog complex organization underlying HR.

    Evidence Co-IP and Ni-affinity pull-downs from human cells expressing tagged paralogs; interaction-hotspot mapping (residues 14–25)

    PMID:11842112 PMID:11842113 PMID:15126333

    Open questions at the time
    • Functional division of labor between BCDX2 and CX3 not defined
    • How RAD51C partitions between the two complexes unknown
  4. 2002 High

    Loss-of-function studies in hamster cells showed RAD51C is required for damage resistance, RAD51 focus formation, sister-chromatid recombination, and formation of both paralog complexes, placing it at the core of cellular HR.

    Evidence Mutant hamster cells (CL-V4B, irs3), clonogenic survival, SCE and chromosomal aberration analysis, RAD51 focus immunofluorescence, specific complementation, Co-IP

    PMID:11912211 PMID:12000837

    Open questions at the time
    • Molecular step within HR not pinpointed
    • Relationship between cohesion defects and recombination not resolved
  5. 2003 High

    Defining the ATP-binding domain and C-terminal NLS as functional determinants connected RAD51C enzymatic activity and nuclear targeting to its requirement for gene-conversion repair of chromosomal DSBs.

    Evidence Site-directed mutagenesis, GFP localization, chromosomal gene-conversion assay with complementation; XRCC3 interface mapping

    PMID:12853621 PMID:12966089

    Open questions at the time
    • Catalytic mechanism of ATP hydrolysis not structurally defined
    • NLS-dependent import pathway not identified
  6. 2004 High

    Immunodepletion/complementation showed RAD51C is required for Holliday-junction branch migration and resolution, and that BCDX2 prefers branched DNA, defining a late HR role in processing recombination intermediates.

    Evidence In vitro HJ resolvase assays with cell extracts, immunodepletion and complementation, BCDX2 substrate-preference and strand-annealing assays; RNAi linking RAD51C to XRCC3 stability and S/G2 radiosensitivity

    PMID:14716019 PMID:15141025 PMID:15292210

    Open questions at the time
    • Identity of the associated nuclease/resolvase not established
    • How RAD51C reaches branched intermediates in cells unclear
  7. 2004 High

    ATPase mutagenesis of XRCC3 and RAD51D showed paralog ATP binding/hydrolysis regulates CX3 assembly/disassembly and is required for HR and paralog interactions, indicating nucleotide-gated complex dynamics.

    Evidence Walker A mutagenesis, complementation in deficient cells, co-purification with ATP/ADP addition, yeast two-hybrid interaction mapping

    PMID:15037616 PMID:16236763

    Open questions at the time
    • RAD51C's own ATPase contribution to complex dynamics not isolated here
    • In vivo nucleotide regulation not directly observed
  8. 2006 High

    Co-elution of HJ resolvase activity with CX3 and RAD51C localization at meiotic crossover sites assigned the resolvase function to the CX3 complex and extended RAD51C to meiotic recombination resolution.

    Evidence Gel filtration, in vitro HJ resolvase assay, immunolocalization with MLH1 on mouse meiotic chromosomes; tract-length analysis of gene conversion

    PMID:16954385 PMID:17114795

    Open questions at the time
    • Resolvase catalytic component within CX3 not defined
    • Mechanism of long-tract suppression not molecularly resolved
  9. 2007 High

    Mouse genetics established RAD51C as essential for viability with sexually dimorphic meiotic defects and reduced HJ resolution, and revealed a role in centrosome maintenance, broadening its in vivo importance.

    Evidence Knockout/hypomorphic mice, meiotic cytology, aneuploidy and HJ resolvase assays in MEFs; centrosome counting in deficient cells

    PMID:17268176 PMID:17312021

    Open questions at the time
    • Centrosome role mechanistically unexplained (idx 20 single observation, no complementation)
    • Cause of male/female meiotic dimorphism unresolved
  10. 2009 High

    RAD51C was placed in damage signaling—required for CHK2 activation and recruited downstream of ATM/NBS1/RPA—and shown to drive BRCA2-independent RAD51 nuclear import and tumor suppression epistatic with Trp53.

    Evidence RNAi with CHK2 phosphorylation and checkpoint readouts, recruitment kinetics with ATM/NBS1/RPA epistasis, subcellular fractionation in BRCA2-defective cells, ATR/CHK1-dependent centrosome amplification, Trp53 cis/trans mouse genetics

    PMID:16215984 PMID:19155299 PMID:19403737 PMID:19451272 PMID:19783859

    Open questions at the time
    • Direct link between RAD51C and CHK2 kinase not biochemically resolved
    • Molecular basis of RAD51 nuclear-import role undefined
  11. 2011 High

    Positioning RAD51C downstream of FANCD2 monoubiquitination but essential for HR in ICL repair clarified its place in the Fanconi anemia pathway and separated HR from signaling defects in disease mutants.

    Evidence RNAi, ICL sensitivity, FANCD2 monoubiquitination and RAD51 focus assays, CHK2 phosphorylation, FA-pathway epistasis with patient mutants

    PMID:22167183

    Open questions at the time
    • Mechanistic coupling of RAD51C to upstream FA core complex unclear
    • Why some mutants separate HR from signaling not structurally explained
  12. 2013 High

    Discovery of a PALB2–RAD51C–BRCA2 complex, with cancer-associated mutations disrupting it, linked RAD51C to the BRCA2/PALB2 mediator axis governing HR capacity.

    Evidence Co-IP, direct binding assays via PALB2 WD40 domain, HR assays with missense mutants

    PMID:24141787

    Open questions at the time
    • Functional consequence of RAD51C–PALB2 binding for filament assembly not defined
    • Relationship to BCDX2/CX3 complexes unresolved
  13. 2018 Medium

    Identifying RAD51C/XRCC3 as mitochondrial nucleoid components required for mtDNA synthesis extended its function to nucleus-independent genome maintenance.

    Evidence Mitochondrial fractionation, mtDNA ChIP, mtDNA synthesis and POLG stability assays, Twinkle helicase dependence by RNAi

    PMID:29158291

    Open questions at the time
    • Mechanism of mtDNA maintenance role single-lab and not reconstituted
    • How nuclear vs mitochondrial pools are partitioned unknown
  14. 2019 Medium

    A direct RAD51C–ALKBH3 interaction that stimulates demethylation repair revealed a function beyond strand exchange in coupling recombination substrates to alkylation-damage reversal.

    Evidence Co-IP, in vitro ALKBH3 demethylation assays, in vivo functional assays with interaction-deficient mutants

    PMID:31642493

    Open questions at the time
    • Single-lab finding without independent replication
    • In vivo relevance to genome stability not fully established
  15. 2023 High

    Cryo-EM and X-ray structures of BCDX2 and CX3 provided the mechanistic basis for RAD51C function—mimicry of RAD51 protomers, coupled ATPase-driven filament nucleation/extension, and a CX3 polymerization motif controlling fork protection/restart/reversal.

    Evidence Cryo-EM, X-ray crystallography with ATP analog, AlphaFold2 modeling, single-molecule RAD51 filament assays, ATPase mutagenesis, CRISPR-edited human cells; double-mutant mouse epistasis with Brca2

    PMID:36906610 PMID:37344587 PMID:37488098

    Open questions at the time
    • Dynamic RAD51B position within BCDX2 not fully resolved
    • How structures explain distinct disease mutant phenotypes incompletely mapped
  16. 2024 High

    Systematic variant mapping (Walker A clustering and saturation genome editing) connected RAD51C residue-level function to HR, paralog interactions, and clinical cancer risk, enabling functional variant classification.

    Evidence HR assays of >50 missense variants with paralog-interaction/ATPase/ssDNA assays; saturation genome editing of 9,188 variants with cell fitness and UK Biobank/ovarian cohort association

    PMID:36099300 PMID:39299233

    Open questions at the time
    • Fitness readout does not resolve which molecular sub-function each variant disrupts
    • Hypomorphic vs null behavior of specific variants not mechanistically dissected
  17. 2010 High

    Biallelic mutation in a consanguineous family defined RAD51C as the Fanconi anemia gene FANCO, establishing the disease consequence of complete RAD51C loss.

    Evidence Gene sequencing, RAD51 focus formation and crosslinker/camptothecin sensitivity in patient-derived cells

    PMID:20400963

    Open questions at the time
    • Genotype–phenotype relationships across FANCO patients not detailed
    • Mechanistic basis of tissue specificity unclear
  18. 2021 High

    Dissecting PARPi response showed RAD51C-deficient synthetic lethality is driven by hyperactivated NHEJ and that reversion mutations or loss of promoter methylation restore HR to drive resistance, defining therapeutic mechanism and escape routes.

    Evidence PARPi treatment with NHEJ chromatin recruitment/activity assays and rescue by KU70/LigIV/DNA-PKcs depletion; tumor and PDX sequencing/methylation with in vitro complementation and modeling

    PMID:25292178 PMID:27753535 PMID:28588062 PMID:34321239

    Open questions at the time
    • Predictors of which patients revert vs demethylate unknown
    • How estrogen/ERα regulation of RAD51C intersects with therapy response unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How RAD51C's molecular sub-functions (filament nucleation, HJ resolution, fork protection, checkpoint signaling, mtDNA and ALKBH3 roles) are individually engaged and regulated in vivo, and which are perturbed by specific clinical variants, remains to be integrated.
  • No unified in vivo model assigning each variant to a specific molecular sub-function
  • Regulation of RAD51C partitioning among complexes and compartments undefined
  • Resolvase catalytic component within CX3 still unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 6 GO:0140097 catalytic activity, acting on DNA 4 GO:0140657 ATP-dependent activity 4 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 2 GO:0005815 microtubule organizing center 2 GO:0005739 mitochondrion 1 GO:0005829 cytosol 1
Pathway
R-HSA-73894 DNA Repair 6 R-HSA-1643685 Disease 4 R-HSA-1640170 Cell Cycle 3 R-HSA-1474165 Reproduction 2 R-HSA-69306 DNA Replication 2
Partners
ALKBH3BRCA2PALB2RAD51RAD51BRAD51DXRCC2XRCC3
Complex memberships
BCDX2 (RAD51B-RAD51C-RAD51D-XRCC2)CX3 (RAD51C-XRCC3)PALB2-RAD51C-BRCA2 complexmitochondrial nucleoid

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 RAD51C was identified as a member of the RAD51 protein family encoding a 376 aa protein. Yeast two-hybrid experiments showed RAD51C binds XRCC3 and RAD51B but not itself, suggesting a mediator/accessory role analogous to yeast Rad55/Rad57. Yeast two-hybrid, cDNA cloning, sequence analysis Nucleic acids research Medium 9469824
2001 RAD51C and XRCC3 copurify as a stable complex from baculovirus-infected insect cells and from HeLa cell endogenous extracts. The purified RAD51C–XRCC3 complex binds single-stranded DNA (but not duplex DNA) to form protein–DNA networks visualized by electron microscopy. Baculovirus co-expression, co-purification, Co-IP from HeLa cells, electron microscopy, DNA-binding assay Proceedings of the National Academy of Sciences of the United States of America High 11459987
2001 The purified XRCC3–RAD51C complex catalyzes homologous pairing in vitro; RAD51C alone also shows homologous pairing activity (though reduced), indicating RAD51C is the catalytic subunit. XRCC3 enhances DNA binding of the complex. Both proteins form filamentous structures with ssDNA as observed by electron microscopy. In vitro homologous pairing assay, electron microscopy, yeast two-hybrid, purified recombinant proteins Proceedings of the National Academy of Sciences of the United States of America High 11331762
2001 RAD51B and RAD51C form a stable heterodimeric complex with ssDNA-binding and ssDNA-stimulated ATPase activities. The RAD51B–RAD51C complex acts as a recombination mediator by partially alleviating RPA competition with RAD51 for ssDNA substrate binding, thereby facilitating RAD51-catalyzed DNA strand exchange. Baculovirus co-expression, in vitro DNA strand exchange assay, ATPase assay, DNA-binding assay Genes & development High 11751636
2001 RAD51B and RAD51C form an endogenous heterocomplex in human cells (HeLa, MCF10A, MCF7). Co-immunoprecipitation showed RAD51C is central to a larger complex containing RAD51B, RAD51D, XRCC2, and XRCC3, but RAD51 was not found in these complexes. Co-immunoprecipitation, immunoaffinity chromatography from insect cells, endogenous Co-IP from human cell lines The Journal of biological chemistry High 11744692
2002 RAD51C participates in two distinct in vivo protein complexes: RAD51B–RAD51C–RAD51D–XRCC2 (BCDX2) and RAD51C–XRCC3 (CX3). XRCC2 and RAD51D co-precipitate with RAD51C but not XRCC3; conversely, XRCC3 pulls down with RAD51C but not XRCC2/RAD51D. RAD51 co-precipitates with XRCC3 (not XRCC2 or RAD51D), suggesting a RAD51–RAD51C–XRCC3 complex. Co-immunoprecipitation from human cells expressing epitope-tagged RAD51 paralogs Nucleic acids research High 11842113
2002 XRCC3 and RAD51C interact directly in human cells. RAD51C (but not XRCC3) interacts with RAD51B, RAD51D, and XRCC2, confirming two paralog complexes. Overexpression of XRCC3 elevates endogenous RAD51C levels, suggesting dimerization stabilizes RAD51C. Ni2+-affinity pull-down from stable human cell lines expressing His6-tagged XRCC3 or RAD51C, Western blotting Nucleic acids research High 11842112
2002 Mammalian RAD51C deficiency (CL-V4B hamster cell mutant with exon 5 deletion) causes hypersensitivity to interstrand crosslinking agents (MMC, cisplatin), alkylating agents, and camptothecin; impaired RAD51 focus formation after DNA damage; increased chromosomal aberrations; reduced sister chromatid exchanges; and a reduced level of sister chromatid cohesion. Cell survival clonogenic assay, immunofluorescence (RAD51 foci), sister chromatid exchange assay, chromosomal aberration analysis, sister chromatid cohesion analysis in Rad51C-mutant hamster cells Nucleic acids research High 12000837
2002 RAD51C (RAD51L2) deficiency in hamster irs3 cells causes reduced sister chromatid exchange, increased isochromatid breaks, and decreased RAD51 focus formation after DNA damage. Complementation was specific to RAD51L2; other RAD51-like genes or RAD51 itself did not rescue. RAD51L2 is required for formation of both RAD51 paralog complexes; neither complex forms in irs3 cells. Complementation assay, sister chromatid exchange, chromosomal aberration analysis, immunofluorescence, Co-immunoprecipitation The Journal of biological chemistry High 11912211
2002 Purified RAD51B and RAD51C proteins bind both single- and double-stranded DNA with preference for 3'-tailed duplexes; both exhibit DNA-stimulated ATPase activity. RAD51C displays ATP-independent DNA duplex destabilization activity (reported as apparent strand exchange). RAD51B–RAD51C heterodimer interacts weakly with RAD51. Baculovirus expression, Ni-NTA pull-down, in vitro DNA-binding assay, ATPase assay, DNA strand exchange assay The Journal of biological chemistry High 12427746
2003 Non-conservative mutation of the putative ATP-binding domain of RAD51C (RAD51L2) severely reduces its function, while a conservative mutation causes partial loss. The C-terminal domain functions as a nuclear localization signal. RAD51L2-deficient cells show significantly reduced homology-directed repair (gene conversion) of a chromosomal DSB, partially restored by ectopic RAD51L2 expression. Site-directed mutagenesis, GFP-tagging and localization imaging, gene conversion assay in RAD51L2-deficient cells, complementation The Journal of biological chemistry High 12966089
2003 Drosophila spn-D encodes a RAD51C ortholog required exclusively during meiosis. Single and double spn-B/spn-D mutants showed no sensitization to DSB-inducing agents (X-rays, MMS) in mitotic cells, indicating meiosis-specific (not somatic) function of this RAD51C ortholog in Drosophila. Genetic mutant analysis, X-ray and MMS sensitivity assays, double mutant epistasis Genetics Medium 14504227
2004 Extracts from cells with RAD51C or XRCC3 mutations have reduced Holliday junction (HJ) resolvase activity. Depletion of RAD51C from fractionated human extracts abolished branch migration and HJ resolution activity, both of which were restored by complementation with RAD51 paralog complexes containing RAD51C. RAD51C is thus required for HJ processing in human cells. In vitro HJ resolvase assay with cell extracts, immunodepletion, complementation with purified complexes Science (New York, N.Y.) High 14716019
2004 RNAi-mediated depletion of RAD51C in human cells reduces homologous recombination frequency and causes XRCC3 protein instability (XRCC3 levels drop sharply upon RAD51C depletion), indicating XRCC3 stability depends on heterodimerization with RAD51C. RAD51C-depleted cells are hypersensitive to MMC and ionizing radiation specifically in S and G2/M phases. siRNA knockdown, HR frequency assay, Western blotting for XRCC3 stability, clonogenic survival, cell-cycle phase-specific radiosensitivity analysis The Journal of biological chemistry High 15292210
2004 The RAD51B–RAD51C–RAD51D–XRCC2 (BCDX2) complex preferentially binds branched DNA structures (Y-shaped DNA and synthetic Holliday junctions) over linear or nicked DNA. The BCDX2 complex also catalyzes strand-annealing between complementary ssDNA molecules. Competitive DNA-binding assay with purified BCDX2 complex and seven DNA substrates, strand-annealing assay Nucleic acids research High 15141025
2004 Residues 14–25 of RAD51C define a protein interaction hotspot used in both XRCC3–RAD51C and RAD51B–RAD51C interactions. Point mutations in this region altered interactions with both XRCC3 and RAD51B in two-hybrid assays. A synthetic peptide from this region fused to a membrane transduction domain inhibited subnuclear RAD51 assembly and sensitized cells to cisplatin. Phage display, yeast two-hybrid with point mutants, cell-permeant peptide inhibition, RAD51 focus formation assay, cisplatin sensitivity Cancer research Medium 15126333
2005 RAD51C depletion in human cells leads to reduced steady-state nuclear RAD51 levels and diminished DNA damage-induced increase in nuclear RAD51. RAD51C contains a functional nuclear localization signal and undergoes damage-induced increase in nuclear accumulation. RAD51C plays a role in regulating RAD51 nuclear entry and ubiquitin-mediated proteasome degradation of RAD51 during recombinational repair. Subcellular fractionation, RNAi knockdown, immunofluorescence, Western blotting for RAD51 levels Journal of cellular biochemistry Medium 16215984
2006 HJ resolvase activity co-elutes with the ~80 kDa RAD51C–XRCC3 complex by gel filtration, indicating CX3 is the active complex. RAD51C localizes to mouse meiotic chromosomes at pachytene/diplotene, co-localizing with MLH1 at crossover sites, implicating RAD51C–XRCC3 in resolution of meiotic recombination intermediates. Gel filtration chromatography, in vitro HJ resolvase assay, immunolocalization on meiotic chromosomes The Journal of biological chemistry High 17114795
2006 RAD51C controls the choice between short-tract and long-tract gene conversion in sister chromatid recombination. Rad51C-deficient CL-V4B cells show biased long-tract gene conversions (bimodal distribution <1 kb or >3.2 kb) that are restored to normal short-tract bias upon Rad51C re-expression, indicating RAD51C suppresses long-tract and gene amplification events. Site-specific chromosomal DSB induction, gene conversion assay, tract-length analysis, complementation with wild-type Rad51C Molecular and cellular biology High 16954385
2007 RAD51C is essential for murine viability (null mice die in early embryogenesis). Hypomorphic Rad51c mice display sexually dimorphic meiotic defects: spermatocytes arrest in early meiotic prophase I (consistent with a role in early RAD51-mediated recombination), while oocytes progress to metaphase I but exhibit precocious sister chromatid separation, aneuploidy, and broken chromosomes at metaphase II. Rad51c-null MEFs show markedly reduced HJ resolution activity. Mouse knockout/hypomorphic allele generation, meiotic cytology, aneuploidy analysis, HJ resolvase assay in MEF extracts The Journal of cell biology High 17312021
2007 RAD51C deficiency in CL-V4B cells increases the number of centrosomes in mitosis, leading to aberrant mitotic spindles, suggesting a role for RAD51C in maintaining correct centrosome numbers. Centrosome counting in RAD51C-deficient CL-V4B cells by immunofluorescence, DSB-induced HR frequency assay Cytogenetic and genome research Medium 17268176
2009 RAD51C is required for activation of checkpoint kinase CHK2 and cell cycle arrest in response to DNA damage. RAD51C accumulates at damage sites concomitantly with RAD51 and is retained after RAD51 disassembly (consistent with early and late function). RAD51C recruitment depends on ATM, NBS1, and RPA, placing it after DNA end resection but before RAD51 assembly. Immunofluorescence (DNA damage foci), RNAi knockdown, CHK2 phosphorylation assay, cell-cycle analysis, epistasis by RNAi co-depletion of ATM/NBS1/RPA The Journal of cell biology High 19451272
2009 Rad51c deficiency leads to embryonic lethality, which is partially rescued on a Trp53-null background. Double-heterozygous cis mice (simultaneous LOH of both Rad51c and Trp53) develop tumors of specialized sebaceous glands (distinct from Trp53-only tumors), establishing direct tumor suppressor function for Rad51c and epistatic interaction with Trp53. Mouse genetics, tumor phenotype analysis, LOH-based double-mutant cis/trans comparison Cancer research High 19155299
2009 RAD51C undergoes damage-induced translocation from cytoplasm to nucleus; RAD51C contains a functional nuclear localization signal. Subcellular fractionation showed that RNAi depletion of RAD51C in HeLa and Capan-1 cells results in lower steady-state nuclear RAD51 levels and diminished damage-induced nuclear RAD51 increase, demonstrating a BRCA2-independent mechanism for RAD51 nuclear entry dependent on RAD51C. Subcellular fractionation, RNAi knockdown, quantitative Western blotting, BRCA2-defective cell line (Capan-1) analysis The Journal of biological chemistry High 19783859
2009 RAD51C deficiency in HCT116 cells leads to centrosome aberrations in an ATR–CHK1-dependent manner and increased aneuploidy. Treatment with caffeine, ATR siRNA, or CHK1 inhibitor/siRNA reduced centrosome aberrations, showing the ATR–CHK1 pathway mediates centrosome amplification in Rad51C-deficient cells. RNAi knockdown, centrosome number analysis, ATR/CHK1 inhibition/siRNA epistasis, γH2AX foci analysis, aneuploidy quantification Nucleic acids research Medium 19403737
2011 RAD51C deficiency causes ICL sensitivity, chromatid-type errors, and G2/M accumulation consistent with Fanconi anemia phenotype. RAD51C is dispensable for ICL unhooking and FANCD2 monoubiquitination but essential for HR, confirming its downstream role in ICL repair. RAD51C also controls intra-S-phase checkpoint through CHK2 activation. Pathological FA and cancer-associated RAD51C mutants show distinct defects in HR versus DNA damage signaling. RNAi knockdown, ICL sensitivity assays, FANCD2 monoubiquitination assay, RAD51 focus formation, cell-cycle analysis, CHK2 phosphorylation assay, epistasis with FA pathway components The Journal of biological chemistry High 22167183
2013 RAD51C is part of a novel protein complex containing PALB2 and BRCA2. The PALB2 WD40 domain directly and independently binds both RAD51C and BRCA2. Breast cancer–associated PALB2 WD40 missense mutants partially disrupt PALB2–RAD51C–BRCA2 complex formation and decrease HR capacity. Cancer-associated RAD51C mutants also show decreased PALB2 complex formation. Co-immunoprecipitation, biochemical binding assays, HR assay, complementation with missense mutants Oncogene High 24141787
2018 RAD51C/XRCC3 localizes to mitochondria as a component of the mitochondrial nucleoid, with nucleus-independent roles in mtDNA maintenance. RAD51C/XRCC3 localizes to the mtDNA D-loop regulatory region along with mitochondrial polymerase POLG, and this recruitment depends on Twinkle helicase. RAD51C/XRCC3-deficient cells exhibit reduced mtDNA synthesis, increased mtDNA lesions, and destabilized POLG on mtDNA. Subcellular fractionation (mitochondrial), ChIP on mtDNA, immunofluorescence, mtDNA synthesis assay, protein stability analysis, Twinkle helicase dependence by RNAi Molecular and cellular biology Medium 29158291
2019 RAD51C directly interacts with the ALKBH3 DNA demethylase. The RAD51C–ALKBH3 interaction stimulates ALKBH3-mediated repair of methyl-adducts in 3'-tailed DNA substrates (which serve as RAD51 recombinase substrates). Loss of this interaction impairs ALKBH3 function both in vitro and in vivo. Co-immunoprecipitation, in vitro ALKBH3 demethylation assay, in vitro and in vivo functional assays with interaction-deficient mutants Nucleic acids research Medium 31642493
2023 Cryo-EM structure of the BCDX2 complex (RAD51B–RAD51C–RAD51D–XRCC2) reveals RAD51C–RAD51D–XRCC2 mimics three RAD51 protomers aligned within a nucleoprotein filament, while RAD51B is highly dynamic. Biochemical and single-molecule analyses show BCDX2 stimulates nucleation and extension of RAD51 filaments on ssDNA in reactions dependent on the coupled ATPase activities of RAD51B and RAD51C. BCDX2 orchestrates RAD51 assembly for replication fork protection and DSB repair. Cryo-electron microscopy, AlphaFold2 modelling, structural proteomics, in vitro RAD51 filament assembly assay, single-molecule analysis, ATPase mutant biochemistry Nature High 37344587
2023 X-ray co-crystal structure of RAD51C–XRCC3 (CX3) with bound ATP analog reveals ATP binding matching RAD51 recombinase, distinct CX3 interfaces, and an unappreciated polymerization motif. Structural analysis combined with CRISPR/Cas9-edited human cells established separable RAD51C functions in DNA replication fork protection, restart, and reversal through discrete CX3 regions for DNA binding and implied 5' RAD51 filament capping. X-ray crystallography, CRISPR/Cas9 genome editing, single-molecule analysis, single-cell assays, biophysics measurements, cancer mutation mapping Nature communications High 37488098
2022 A cluster of RAD51C missense mutations in and around the Walker A (ATP-binding) box disrupts HR, interactions with multiple RAD51 paralogs (RAD51B, RAD51D, XRCC2), ssDNA binding, and ATP hydrolysis. Structural modeling predicts ATP binding at the interface of RAD51C with other RAD51 paralogs, explaining how Walker A mutations simultaneously disrupt multiple paralog interactions. HR functional assay (>50 missense variants), protein interaction assays with paralog complexes, ssDNA binding assay, ATPase assay, structural modeling Proceedings of the National Academy of Sciences of the United States of America High 36099300
2024 Saturation genome editing (SGE) functionally assessed 9,188 unique RAD51C variants (>99.5% of all possible coding sequence SNVs). 3,094 variants were classified as disruptive based on cell fitness changes. Cell fitness was the primary readout. Specific missense variants showed distinct depletion kinetics suggesting hypomorphic alleles. Critical residues mapped onto the RAD51C structure; SGE-depleted variants associated with cancer diagnoses in UK Biobank. Saturation genome editing, Gaussian mixture modeling of variant abundance, UK Biobank and ovarian cancer cohort association Cell High 39299233
2003 XRCC3 residues Tyr139 and Phe249 are essential for RAD51C binding. The Rad51C-binding region of XRCC3 spans amino acids 63–346. The XRCC3(63-346)–RAD51C complex retains ssDNA and dsDNA binding activities comparable to the full-length complex. Yeast two-hybrid, protein purification, in vitro binding assay, DNA-binding assay with truncation/point mutants Nucleic acids research Medium 12853621
2004 XRCC3 ATPase activity (Walker A box) is required for homologous recombination complementation and for normal XRCC3–RAD51C complex dynamics. Wild-type and K113A mutant XRCC3 form stable complexes with RAD51C; K113R mutant does not (predominantly insoluble). Addition of ATP (but not ADP) abolishes complex formation, suggesting ATP binding/hydrolysis by XRCC3 regulates CX3 complex assembly/disassembly. Site-directed mutagenesis, complementation assay in XRCC3-deficient CHO cells, co-expression in bacteria with Ni-affinity co-purification, ATP/ADP addition experiment The Journal of biological chemistry High 15037616
2005 The ATPase motif of RAD51D (Walker A K113) is required for resistance to DNA interstrand crosslinks; K113R and K113A mutations caused 96% and 83% reduction in repair capacity. Walker A mutations in RAD51D reduced interaction with RAD51C ~8-fold in yeast two-hybrid assays while XRCC2 interaction was retained, demonstrating the RAD51D ATPase is required for its interaction with RAD51C. Site-directed mutagenesis, complementation assay in Rad51d-null MEFs, yeast two-hybrid interaction analysis Mutagenesis Medium 16236763
2010 Biallelic RAD51C missense mutation in a consanguineous family caused loss of RAD51 focus formation in response to DNA damage and increased cellular sensitivity to MMC and camptothecin, establishing RAD51C as a Fanconi anemia–like disorder gene (FANCO). Whole-exome/gene sequencing, RAD51 focus formation assay (immunofluorescence), cellular crosslinker and topoisomerase inhibitor sensitivity assays Nature genetics High 20400963
2017 Secondary somatic mutations in RAD51C that restore the open reading frame confer resistance to PARP inhibitor rucaparib in ovarian carcinoma. In vitro complementation assays confirmed that secondary RAD51C mutations restore HR function and drive PARPi resistance. Molecular modeling predicted functional restoration of RAD51C protein by secondary mutations. Tumor biopsy sequencing (pre/post treatment), in vitro complementation assays, patient-derived xenograft, predictive molecular modeling Cancer discovery High 28588062
2021 RAD51C promoter methylation (homozygous) silences RAD51C expression, causes homologous recombination deficiency, and confers PARP inhibitor sensitivity. Loss of a single unmethylated RAD51C gene copy is sufficient to drive PARPi resistance; loss of RAD51C promoter methylation under PARPi treatment pressure was confirmed as a resistance mechanism in PDX models. Patient-derived xenograft (PDX) models, methylation analysis, RAD51C mRNA quantification, SNP array copy number profiling, PARPi treatment experiments Cancer research High 34321239
2016 Estrogen transcriptionally upregulates RAD51C expression in an ERα-dependent manner in ERα-positive breast cancer cells. Estrogen also induces RAD51C assembly into nuclear foci at DSBs, which precedes RAD51 complex recruitment. Anti-estrogens or ERα siRNA prevent estrogen-induced RAD51C upregulation. Reporter assay, qRT-PCR, immunofluorescence (RAD51C foci), siRNA knockdown of ERα, anti-estrogen treatment Cell cycle (Georgetown, Tex.) Medium 27753535
2014 RAD51C-deficient cells treated with PARP inhibitor show enhanced non-homologous end joining (NHEJ) protein recruitment to chromatin, increased error-prone NHEJ activity, and synthetic lethality. Inhibition of DNA-PKcs or depletion of KU70 or Ligase IV rescues cell death, demonstrating that PARPi-induced synthetic lethality in RAD51C-deficient cells is mediated by hyperactivated NHEJ. PARP inhibitor treatment, chromatin fractionation (NHEJ protein recruitment), NHEJ activity assay, RNAi knockdown of NHEJ factors, clonogenic survival, G2/M analysis Carcinogenesis Medium 25292178
2023 Combining hypomorphic Brca2/Fancd1 and Rad51c/Fanco mutations in mice phenocopies human Fanconi anemia (bone marrow failure, rapid cancer death, drug hypersensitivity, severe replication instability), while single-gene mutations produce unremarkable phenotypes. This demonstrates unexpected synergism between FANC mutations (polygenic replication stress concept) and places RAD51C/FANCO in an epistatic relationship with BRCA2/FANCD1 in replication stress response. Mouse double-mutant genetics, bone marrow failure analysis, tumor spectrum analysis, cancer drug hypersensitivity assays, replication instability assays Nature communications High 36906610

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Germline mutations in breast and ovarian cancer pedigrees establish RAD51C as a human cancer susceptibility gene. Nature genetics 543 20400964
2017 Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma. Cancer discovery 341 28588062
2010 Mutation of the RAD51C gene in a Fanconi anemia-like disorder. Nature genetics 319 20400963
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 258 26261251
2004 RAD51C is required for Holliday junction processing in mammalian cells. Science (New York, N.Y.) 245 14716019
2001 Mediator function of the human Rad51B-Rad51C complex in Rad51/RPA-catalyzed DNA strand exchange. Genes & development 193 11751636
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 153 29361001
1998 Isolation and characterization of RAD51C, a new human member of the RAD51 family of related genes. Nucleic acids research 142 9469824
2002 Mammalian Rad51C contributes to DNA cross-link resistance, sister chromatid cohesion and genomic stability. Nucleic acids research 124 12000837
2014 Clinical characteristics of ovarian cancer classified by BRCA1, BRCA2, and RAD51C status. Scientific reports 123 24504028
2013 RAD51C-deficient cancer cells are highly sensitive to the PARP inhibitor olaparib. Molecular cancer therapeutics 119 23512992
2001 Complex formation by the human RAD51C and XRCC3 recombination repair proteins. Proceedings of the National Academy of Sciences of the United States of America 111 11459987
2002 Involvement of Rad51C in two distinct protein complexes of Rad51 paralogs in human cells. Nucleic acids research 110 11842113
2001 Homologous-pairing activity of the human DNA-repair proteins Xrcc3.Rad51C. Proceedings of the National Academy of Sciences of the United States of America 108 11331762
2011 RAD51C is a susceptibility gene for ovarian cancer. Human molecular genetics 107 21616938
2007 RAD51C deficiency in mice results in early prophase I arrest in males and sister chromatid separation at metaphase II in females. The Journal of cell biology 107 17312021
2013 Breast cancer-associated missense mutants of the PALB2 WD40 domain, which directly binds RAD51C, RAD51 and BRCA2, disrupt DNA repair. Oncogene 105 24141787
2016 Germline Mutations in PALB2, BRCA1, and RAD51C, Which Regulate DNA Recombination Repair, in Patients With Gastric Cancer. Gastroenterology 100 28024868
2002 Complex formation by the human Rad51B and Rad51C DNA repair proteins and their activities in vitro. The Journal of biological chemistry 100 12427746
2002 Interactions involving the Rad51 paralogs Rad51C and XRCC3 in human cells. Nucleic acids research 97 11842112
2006 Role of RAD51C and XRCC3 in genetic recombination and DNA repair. The Journal of biological chemistry 92 17114795
2012 Constitutive promoter methylation of BRCA1 and RAD51C in patients with familial ovarian cancer and early-onset sporadic breast cancer. Human molecular genetics 88 22843497
2002 Role of mammalian RAD51L2 (RAD51C) in recombination and genetic stability. The Journal of biological chemistry 87 11912211
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 85 32359370
2010 RAD51C: a novel cancer susceptibility gene is linked to Fanconi anemia and breast cancer. Carcinogenesis 85 20952512
2021 Acquired RAD51C Promoter Methylation Loss Causes PARP Inhibitor Resistance in High-Grade Serous Ovarian Carcinoma. Cancer research 81 34321239
2009 Loss of Rad51c leads to embryonic lethality and modulation of Trp53-dependent tumorigenesis in mice. Cancer research 78 19155299
2000 17q23 amplifications in breast cancer involve the PAT1, RAD51C, PS6K, and SIGma1B genes. Cancer research 78 11034073
2011 BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer. Breast cancer research and treatment 75 21409391
2009 Cellular redistribution of Rad51 in response to DNA damage: novel role for Rad51C. The Journal of biological chemistry 75 19783859
2001 RAD51C interacts with RAD51B and is central to a larger protein complex in vivo exclusive of RAD51. The Journal of biological chemistry 75 11744692
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
2003 The Drosophila spn-D gene encodes a RAD51C-like protein that is required exclusively during meiosis. Genetics 71 14504227
2012 Predominance of pathogenic missense variants in the RAD51C gene occurring in breast and ovarian cancer families. Human molecular genetics 70 22451500
2011 Distinct roles of FANCO/RAD51C protein in DNA damage signaling and repair: implications for Fanconi anemia and breast cancer susceptibility. The Journal of biological chemistry 70 22167183
2009 RAD51C facilitates checkpoint signaling by promoting CHK2 phosphorylation. The Journal of cell biology 70 19451272
2006 Differential regulation of short- and long-tract gene conversion between sister chromatids by Rad51C. Molecular and cellular biology 62 16954385
2023 Structure and function of the RAD51B-RAD51C-RAD51D-XRCC2 tumour suppressor. Nature 58 37344587
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 58 36162851
2017 Clinical characteristics and outcomes of patients with BRCA1 or RAD51C methylated versus mutated ovarian carcinoma. Gynecologic oncology 55 29233532
2009 The development of RAD51C, Cystatin A, p53 and Nrf2 luciferase-reporter assays in metabolically competent HepG2 cells for the assessment of mechanism-based genotoxicity and of oxidative stress in the early research phase of drug development. Mutation research 55 20006733
2013 Oversized AAV transductifon is mediated via a DNA-PKcs-independent, Rad51C-dependent repair pathway. Molecular therapy : the journal of the American Society of Gene Therapy 54 23939025
2011 RAD51C germline mutations in breast and ovarian cancer cases from high-risk families. PloS one 54 21980511
2011 Analysis of RAD51C germline mutations in high-risk breast and ovarian cancer families and ovarian cancer patients. Human mutation 54 21990120
2004 Human Rad51C deficiency destabilizes XRCC3, impairs recombination, and radiosensitizes S/G2-phase cells. The Journal of biological chemistry 51 15292210
2003 Identification of functional domains in the RAD51L2 (RAD51C) protein and its requirement for gene conversion. The Journal of biological chemistry 46 12966089
2011 Further evidence for the contribution of the RAD51C gene in hereditary breast and ovarian cancer susceptibility. Breast cancer research and treatment 43 21750962
2018 RAD51C/XRCC3 Facilitates Mitochondrial DNA Replication and Maintains Integrity of the Mitochondrial Genome. Molecular and cellular biology 42 29158291
2015 Genetic testing for RAD51C mutations: in the clinic and community. Clinical genetics 38 25470109
2010 Screening RAD51C nucleotide alterations in patients with a family history of breast and ovarian cancer. Breast cancer research and treatment 36 20697805
2014 Enhanced non-homologous end joining contributes toward synthetic lethality of pathological RAD51C mutants with poly (ADP-ribose) polymerase. Carcinogenesis 34 25292178
2012 Germline RAD51C mutations in ovarian cancer susceptibility. Clinical genetics 34 22725699
2024 High-resolution functional mapping of RAD51C by saturation genome editing. Cell 33 39299233
2021 Characterization of a RAD51C-silenced high-grade serous ovarian cancer model during development of PARP inhibitor resistance. NAR cancer 33 34316715
2023 RAD51C-XRCC3 structure and cancer patient mutations define DNA replication roles. Nature communications 32 37488098
2012 The rice RAD51C gene is required for the meiosis of both female and male gametocytes and the DNA repair of somatic cells. Journal of experimental botany 31 22859673
2011 A HRM-based screening method detects RAD51C germ-line deleterious mutations in Spanish breast and ovarian cancer families. Breast cancer research and treatment 31 21537932
2014 RAD51C germline mutations found in Spanish site-specific breast cancer and breast-ovarian cancer families. Breast cancer research and treatment 28 25086635
2005 Cellular localization of human Rad51C and regulation of ubiquitin-mediated proteolysis of Rad51. Journal of cellular biochemistry 28 16215984
2019 Combined Tumor Sequencing and Case-Control Analyses of RAD51C in Breast Cancer. Journal of the National Cancer Institute 27 30949688
2019 Human RAD51 paralogue RAD51C fosters repair of alkylated DNA by interacting with the ALKBH3 demethylase. Nucleic acids research 26 31642493
2014 Deleterious RAD51C germline mutations rarely predispose to breast and ovarian cancer in Pakistan. Breast cancer research and treatment 26 24800917
2005 The ATPase motif in RAD51D is required for resistance to DNA interstrand crosslinking agents and interaction with RAD51C. Mutagenesis 26 16236763
2010 Rad51C is essential for embryonic development and haploinsufficiency causes increased DNA damage sensitivity and genomic instability. Mutation research 25 20471405
2022 Homologous recombination-deficient mutation cluster in tumor suppressor RAD51C identified by comprehensive analysis of cancer variants. Proceedings of the National Academy of Sciences of the United States of America 24 36099300
2013 RAD51C deletion screening identifies a recurrent gross deletion in breast cancer and ovarian cancer families. Breast cancer research : BCR 24 24359560
2004 XRCC3 ATPase activity is required for normal XRCC3-Rad51C complex dynamics and homologous recombination. The Journal of biological chemistry 23 15037616
2021 Recurrent Mutations in BRCA1, BRCA2, RAD51C, PALB2 and CHEK2 in Polish Patients with Ovarian Cancer. Cancers 21 33670479
2016 Identification of six pathogenic RAD51C mutations via mutational screening of 1228 Danish individuals with increased risk of hereditary breast and/or ovarian cancer. Breast cancer research and treatment 21 26740214
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
2013 RAD51C--a new human cancer susceptibility gene for sporadic squamous cell carcinoma of the head and neck (HNSCC). Oral oncology 20 24315737
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
2012 Evaluation of RAD51C as cancer susceptibility gene in a large breast-ovarian cancer patient population referred for genetic testing. Breast cancer research and treatment 18 22370629
2009 The ATR-Chk1 pathway plays a role in the generation of centrosome aberrations induced by Rad51C dysfunction. Nucleic acids research 18 19403737
2007 RAD51C (RAD51L2) is involved in maintaining centrosome number in mitosis. Cytogenetic and genome research 18 17268176
2020 Comprehensive Functional Characterization and Clinical Interpretation of 20 Splice-Site Variants of the RAD51C Gene. Cancers 17 33333735
2007 Resolving RAD51C function in late stages of homologous recombination. Cell division 17 17547768
2003 Region and amino acid residues required for Rad51C binding in the human Xrcc3 protein. Nucleic acids research 17 12853621
2012 Mutation screening of RAD51C in high-risk breast and ovarian cancer families. Familial cancer 16 22476429
2017 Characterisation of the novel deleterious RAD51C p.Arg312Trp variant and prioritisation criteria for functional analysis of RAD51C missense changes. British journal of cancer 15 28829762
2024 Prevalence of Homologous Recombination Deficiency Among Patients With Germline RAD51C/D Breast or Ovarian Cancer. JAMA network open 14 38648056
2017 Mutation status of RAD51C, PALB2 and BRIP1 in 100 Japanese familial breast cancer cases without BRCA1 and BRCA2 mutations. Cancer science 14 28796317
2015 Identification of a breast cancer family double heterozygote for RAD51C and BRCA2 gene mutations. Familial cancer 14 25154786
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
2004 A hot spot for RAD51C interactions revealed by a peptide that sensitizes cells to cisplatin. Cancer research 14 15126333
2004 Spontaneous homologous recombination is decreased in Rad51C-deficient hamster cells. DNA repair 14 15336628
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
2017 Expanding the FANCO/RAD51C associated phenotype: Cleft lip and palate and lobar holoprosencephaly, two rare findings in Fanconi anemia. European journal of medical genetics 13 29278735
2017 Pathologic findings in breast, fallopian tube, and ovary specimens in non-BRCA hereditary breast and/or ovarian cancer syndromes: a study of 18 patients with deleterious germline mutations in RAD51C, BARD1, BRIP1, PALB2, MUTYH, or CHEK2. Human pathology 12 28709830
2016 Estrogen induces RAD51C expression and localization to sites of DNA damage. Cell cycle (Georgetown, Tex.) 12 27753535
2001 Sequence, chromosomal location and expression analysis of the murine homologue of human RAD51L2/RAD51C. Gene 12 11410366
2023 Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C. Cancer research 11 37253112
2022 Minigene Splicing Assays Identify 20 Spliceogenic Variants of the Breast/Ovarian Cancer Susceptibility Gene RAD51C. Cancers 11 35740625
2018 Gene-panel testing of breast and ovarian cancer patients identifies a recurrent RAD51C duplication. Clinical genetics 11 28802053
2013 C. elegans ring finger protein RNF-113 is involved in interstrand DNA crosslink repair and interacts with a RAD51C homolog. PloS one 11 23555887
2023 Hypomorphic Brca2 and Rad51c double mutant mice display Fanconi anemia, cancer and polygenic replication stress. Nature communications 10 36906610
2021 TAZ maintains telomere length in TNBC cells by mediating Rad51C expression. Breast cancer research : BCR 10 34488828
2012 Screening of Finnish RAD51C founder mutations in prostate and colorectal cancer patients. BMC cancer 10 23176254
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

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