Affinage

RAD54L

DNA repair and recombination protein RAD54-like · UniProt Q92698

Round 2 corrected
Length
747 aa
Mass
84.4 kDa
Annotated
2026-04-28
58 papers in source corpus 15 papers cited in narrative 15 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAD54L is a SWI2/SNF2-family ATPase that functions downstream of RAD51 in homologous recombination, where it resolves RAD51/MND1-containing filaments during homology search, promotes strand invasion, and operates in two distinct RAD51-dependent replication fork reversal pathways—one HLTF/SMARCAL1-dependent (branch migration-dispensable) and one FBH1-dependent (branch migration-essential)—to restrain fork progression and suppress replication-associated ssDNA gaps (PMID:39315725, PMID:35652094). RAD54L defines a non-redundant HR sub-pathway parallel to RAD51AP1, and its loss synergistically sensitizes cells to PARP inhibitors, mitomycin C, and hydroxyurea (PMID:35652094). RAD54L physically interacts with p53 via the p53 C-terminus and co-localizes with RAD51 at DNA damage sites, integrating HR with p53-mediated anti-recombinogenic control (PMID:12750285). Its expression is transcriptionally regulated by E2F1, CHEK1, CDC7, Oct4, and SOHLH2, linking HR repair capacity to radioresistance in multiple cancer types (PMID:33261027, PMID:29287241, PMID:41535248).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2001 High

    The question of whether RAD54L-dependent HR contributes to DSB repair in mammalian cells was addressed by showing that dominant-negative RAD54L increases radiation sensitivity and chromosomal aberrations only when the primary NHEJ pathway (DNA-PKcs) is inactivated, establishing HR as a backup DSB repair route whose contribution is masked by NHEJ.

    Evidence Dominant-negative hRAD54 expression in SCID (DNA-PK-deficient) cells with IR sensitivity, PFGE, and chromosome aberration analysis

    PMID:11289143

    Open questions at the time
    • Whether RAD54L enzymatic activity (ATPase/branch migration) is specifically required was not dissected
    • Contribution of RAD54L to HR in non-transformed human cells was not tested
  2. 2003 High

    The nature of RAD54L's interaction with p53 and RAD51 was clarified: RAD54L co-immunoprecipitates with both p53 and RAD51 at endogenous levels, binds p53's C-terminus directly in vitro, and co-localizes at DNA processing sites, placing RAD54L within the p53-regulated HR complex.

    Evidence Co-IP, GST pulldown for direct binding, immunofluorescence co-localization, and host-cell reactivation recombination assay in human cells

    PMID:12750285

    Open questions at the time
    • Structural basis of the p53–RAD54L interaction is unknown
    • Functional consequence of disrupting the p53–RAD54L interaction specifically (vs. p53–RAD51) was not separated
  3. 2005 Medium

    RAD54L-dependent HR was shown to mediate the aberrant telomere elongation observed in SCID cells, extending RAD54L's functional scope beyond canonical DSB repair to telomere maintenance.

    Evidence Dominant-negative RAD54L in SCID cells with telomere length measurement and CO-FISH for telomeric recombination

    PMID:15975611

    Open questions at the time
    • Whether RAD54L acts at telomeres in wild-type cells with functional DNA-PKcs is unknown
    • Mechanism by which HR elongates telomeres in SCID cells was not molecularly resolved
  4. 2015 Medium

    Beyond its repair role, RAD54L was identified as a potential oncogene gained in choroid plexus carcinoma, with functional knockdown demonstrating its requirement for CPC initiation and progression—expanding RAD54L's disease relevance beyond DNA repair deficiency.

    Evidence Cross-species syntenic genome analysis plus functional knockdown in mouse CPC model and human CPC cell lines

    PMID:25965574

    Open questions at the time
    • Mechanism by which RAD54L promotes tumorigenesis (repair-dependent vs. repair-independent) was not resolved
    • Whether this oncogenic role extends to other tumor types was not determined
  5. 2017 Medium

    Upstream transcriptional control of RAD54L began to be mapped: CHEK1 and subsequently CDC7 were shown to regulate RAD54L promoter activity in glioblastoma, establishing kinase-to-transcription axes that modulate HR capacity and radioresistance.

    Evidence siRNA knockdown of CHEK1/CDC7, luciferase reporter assays for RAD54L promoter, clonogenic survival after IR, xenograft models

    PMID:29287241 PMID:29413763

    Open questions at the time
    • Whether CHEK1 and CDC7 act on the same or distinct cis-elements in the RAD54L promoter is unknown
    • Direct transcription factor intermediaries between these kinases and the RAD54L promoter were not identified
  6. 2020 Medium

    E2F1 was shown to directly bind the RAD54L promoter and transcriptionally induce RAD54L expression, with the resulting RAD54L mediating HR repair of mitomycin C-induced DSBs in bladder cancer, providing the first direct transcription factor–promoter interaction driving RAD54L in cancer.

    Evidence ChIP for E2F1 at RAD54L promoter, siRNA knockdown, mitomycin C DNA damage repair assays in bladder cancer cells

    PMID:33261027

    Open questions at the time
    • Whether E2F1 is the dominant transcriptional regulator of RAD54L or cooperates with CHEK1/CDC7-regulated factors is unclear
    • Chromatin context and epigenetic modulation of the RAD54L promoter were not examined
  7. 2022 High

    Genetic epistasis analysis using CRISPR double knockouts established that RAD54L and RAD51AP1 define two parallel, non-redundant HR sub-pathways downstream of RAD51, with concomitant loss producing synergistic sensitivity to olaparib, mitomycin C, and hydroxyurea.

    Evidence CRISPR/Cas9 double KO of RAD51AP1 and RAD54L in human cancer cells, multi-agent drug sensitivity assays

    PMID:35652094

    Open questions at the time
    • Substrate or intermediate specificity distinguishing the two sub-pathways is not defined
    • Whether RAD54B fully substitutes for RAD54L in specific genomic contexts was not resolved
  8. 2024 High

    RAD54L was shown to function as a replication fork remodeler that restrains fork progression and suppresses ssDNA gaps under replication stress, acting in two mechanistically distinct RAD51-mediated fork reversal pathways—one with HLTF/SMARCAL1 (branch migration dispensable) and one with FBH1 (branch migration essential)—resolving a longstanding question about how RAD54L's ATPase and branch migration activities are differentially deployed.

    Evidence DNA fiber assays, genetic epistasis with HLTF/SMARCAL1/FBH1 KO, branch migration-deficient RAD54L mutant, nascent strand degradation in BRCA1/2- and 53BP1-deficient backgrounds

    PMID:39315725

    Open questions at the time
    • Structural basis for differential engagement of RAD54L in the two fork reversal pathways is unknown
    • Whether the fork remodeling function is relevant in non-replicating or quiescent cells was not tested
  9. 2025 Medium

    Live-cell imaging directly visualized RAD54L's requirement for resolution of RAD51/MND1-containing filaments during homology search, placing RAD54L at the transition from homology search to strand invasion in living human cells.

    Evidence Live-cell imaging with GFP-MND1, RAD54L siRNA/knockout, time-lapse microscopy of filament dynamics (preprint)

    PMID:bio_10.1101_2025.03.01.640932

    Open questions at the time
    • Whether RAD54L's ATPase or branch migration activity drives filament resolution is not distinguished
    • Awaits peer review and independent replication
  10. 2025 Medium

    A CRISPR synthetic lethal screen revealed an unexpected protective role for RAD54L in nucleolar rDNA surveillance: RAD54L loss increases nucleolar R-loops, rDNA damage, and sensitivity to PARP and RNA Pol I inhibitors, extending RAD54L function to the nucleolar DNA damage response.

    Evidence CRISPR-Cas9 screen with RNA Pol I inhibitors, RAD54L KO, DRIP for R-loops, rDNA damage and nucleolar structure assays (preprint)

    PMID:bio_10.1101_2025.01.20.633984

    Open questions at the time
    • Whether RAD54L acts directly on rDNA or indirectly via general HR at the nucleolus is unclear
    • Awaits peer review and independent validation
  11. 2026 Medium

    SOHLH2 was identified as a transcriptional activator of RAD54L in NSCLC, with RAD54L overexpression fully rescuing HR repair and radioresistance upon SOHLH2 loss, confirming a direct SOHLH2→RAD54L transcriptional axis.

    Evidence ChIP for SOHLH2 at RAD54L promoter, rescue overexpression experiments, HR repair and clonogenic survival assays

    PMID:41535248

    Open questions at the time
    • Whether SOHLH2 cooperates with E2F1 or other transcription factors at the RAD54L promoter is unknown
    • Relevance of the SOHLH2–RAD54L axis in non-malignant tissues is not examined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for RAD54L's differential engagement in fork reversal vs. DSB repair vs. nucleolar rDNA surveillance; whether RAD54L's repair-independent oncogenic function in CPC and other tumors depends on its ATPase/branch migration activities; and how the multiple transcriptional inputs (E2F1, CHEK1, CDC7, Oct4, SOHLH2) are integrated at the RAD54L promoter in physiological contexts.
  • No structure of human RAD54L in complex with its substrates or partners
  • Repair-dependent vs. repair-independent oncogenic mechanisms not separated
  • Integrated promoter logic for RAD54L regulation across cell types not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 2 GO:0140097 catalytic activity, acting on DNA 2 GO:0140657 ATP-dependent activity 1
Localization
GO:0005634 nucleus 2 GO:0005730 nucleolus 1
Pathway
R-HSA-73894 DNA Repair 5 R-HSA-1640170 Cell Cycle 1 R-HSA-69306 DNA Replication 1
Partners
FBH1HLTFMND1RAD51RAD51AP1SMARCAL1TP53

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 p53, hRAD51, and hRAD54 (RAD54L) co-immunoprecipitate and co-localize at endogenous levels in normal cells, with co-localization at DNA processing sites after DNA breaks. hRAD54 binds directly to the p53 C-terminus in vitro without a nucleic acid intermediate. Functionally, p53-dependent anti-recombinogenic activity was attributed to p53 binding to hRAD51, and the elevation in recombination upon p53 inactivation is dependent on the hRAD51 pathway, placing RAD54L in the p53-regulated HR pathway. Co-immunoprecipitation, co-localization (immunofluorescence), direct binding assay in vitro (GST pulldown), host cell reactivation assay for recombination Cancer research High 12750285
2001 Expression of a dominant-negative mutant hRAD54 in DNA-PK-deficient (SCID) cells created double-mutant cells with increased ionizing radiation sensitivity, reduced DSB repair, and numerous incomplete chromatid exchange aberrations compared to either single mutant alone. Single-mutant hRAD54 cells showed wild-type phenotype, indicating that HR (RAD54L-dependent) is not apparent for DSB repair unless the primary NHEJ pathway is non-functional. Additionally, DNA-PK-null cells were more resistant to mitomycin-C than wild-type, suggesting HR is more efficient for cross-link repair in the absence of NHEJ. Dominant-negative mutant expression in SCID cell lines, ionizing radiation sensitivity assays, pulsed-field gel electrophoresis for DSB repair, chromosome aberration analysis, mitomycin-C survival assay Cancer research High 11289143
2005 Expression of dominant-negative mutant hRAD54 in SCID cells reversed the abnormal telomere elongation characteristic of SCID cells and significantly reduced recombination rates at telomeres (measured by CO-FISH). This paralleled the effect of restoring functional DNA-PKcs, establishing that telomere elongation in SCID cells results from interactions between homologous recombination (RAD54L-dependent) and DNA-PKcs activity. Dominant-negative mutant hRAD54 expression in SCID cells, telomere length measurement, chromosome orientation FISH (CO-FISH) to measure telomeric recombination rates Mutation research Medium 15975611
2015 RAD54L was identified as an oncogene co-located on human chromosome 1p32-35.3 and required for choroid plexus carcinoma (CPC) initiation and progression in both mouse and human tumors. Cross-species genomic analysis identified RAD54L as gained in tumors, and functional experiments established its necessity for disease progression, distinct from its known DNA repair role. Cross-species genome-wide syntenic region analysis, functional knockdown in mouse CPC model and human CPC cell lines, genomic copy number analysis Cancer cell Medium 25965574
2017 CHEK1 (Checkpoint kinase 1) regulates RAD54L expression via regulation of RAD54L promoter activity in glioblastoma cells. CHEK1 knockdown reduced RAD54L expression, increased apoptosis when combined with radiotherapy, and CHEK1 inhibition attenuated tumor growth, placing RAD54L downstream of CHEK1 in a transcriptional regulatory axis that promotes radioresistance. siRNA knockdown of CHEK1, luciferase reporter assays for RAD54L promoter activity, clonogenic survival assays, in vitro and in vivo tumor growth assays Translational oncology Medium 29287241
2018 CDC7 kinase regulates RAD54L expression by controlling RAD54L promoter activity in glioblastoma. CDC7 knockdown reduced RAD54L levels, attenuated radioresistance, and CDC7 inhibitor reduced tumor growth both in vitro and in vivo, establishing a CDC7→RAD54L transcriptional axis in GBM radioresistance. siRNA knockdown of CDC7, luciferase reporter assay for RAD54L promoter, clonogenic survival after irradiation, in vivo xenograft tumor growth Translational oncology Medium 29413763
2020 E2F1 directly binds to the promoter region of RAD54L and transcriptionally regulates RAD54L expression in bladder cancer cells. RAD54L induced by E2F1 mediates repair of DNA double-strand breaks caused by mitomycin C via the homologous recombination repair pathway. ChIP assay demonstrating E2F1 binding to RAD54L promoter, gene expression analysis, siRNA knockdown, DNA damage repair assays with mitomycin C International journal of molecular sciences Medium 33261027
2021 The CSC-related transcription factor Oct4 A transcriptionally regulates RAD54L expression in head and neck squamous cell carcinoma. Knockdown of Oct4 A led to downregulation of RAD54L (and PSMC3IP), resulting in reduced self-renewal capacity and partial radiosensitization. Knockdown of RAD54L itself also reduced self-renewal and clonogenic survival after irradiation, directly linking RAD54L to HR-mediated repair and the cancer stem cell phenotype. Oct4 A siRNA knockdown, RAD54L siRNA knockdown, clonogenic survival assays after irradiation, self-renewal (sphere formation) assays, gene expression analysis Oncogene Medium 34079088
2022 RAD51AP1 and RAD54L define two distinct RAD51-dependent HR sub-pathways that function downstream of RAD51 recombinase. Concomitant deletion of RAD51AP1 and RAD54L synergistically sensitizes human cancer cells to olaparib, mitomycin C, and hydroxyurea beyond either single deletion. The RAD54L paralog RAD54B compensates for RAD54L deficiency, but less extensively than RAD51AP1, delineating non-redundant compensatory sub-pathways. CRISPR/Cas9 double knockout of RAD51AP1 and RAD54L, drug sensitivity assays (olaparib, mitomycin C, hydroxyurea), genetic epistasis analysis Frontiers in cell and developmental biology High 35652094
2022 High RAD54L expression in bladder cancer promotes abnormal tumor cell proliferation by altering cell cycle progression and suppressing cellular senescence. RAD54L expression is associated with p53, p21, and pRB levels in bladder cancer tissue, suggesting RAD54L modulates cell cycle checkpoint pathways. RAD54L knockdown, cell cycle analysis by flow cytometry, senescence assays (SA-β-gal staining), Western blotting for p53/p21/pRB Medical oncology Low 36071250
2024 RAD54L restrains replication fork progression and functions as a fork remodeler in human cancer cell lines and non-transformed cells. RAD54L decelerates fork progression under replication stress and suppresses replication-associated ssDNA gaps. RAD54L functions in two distinct RAD51-mediated fork reversal pathways: (1) In the HLTF/SMARCAL1 pathway, RAD54L is critical but its branch migration activity is dispensable, placing it downstream of HLTF/SMARCAL1; (2) In the FBH1 pathway, RAD54L's branch migration activity is essential, and FBH1 engagement depends on concerted action with RAD54L. Loss of RAD54L prevents nascent strand degradation in BRCA1/2- and 53BP1-deficient cells. DNA fiber assays (fork progression, ssDNA gap analysis), genetic epistasis with HLTF/SMARCAL1/FBH1 knockouts, branch migration-deficient RAD54L mutant, nascent strand degradation assays in BRCA1/2- and 53BP1-deficient backgrounds Nucleic acids research High 39315725
2024 In a Fragile X repeat expansion mouse model, loss of Rad54l (alone) did not significantly affect CGG repeat expansion, establishing by genetic epistasis that RAD54L-dependent HR pathways are not required for microsatellite repeat expansion in this context. Rad54l knockout mouse embryonic stem cells, repeat expansion assay by Southern blot/PCR, genetic epistasis with Rad52, Rad54b, Pol θ bioRxivpreprint Low 39574643
2025 RAD54L plays a protective role in the nucleolar DNA damage response (nDDR). Loss of RAD54L increases nucleolar R-loops and rDNA damage, causes defects in nucleolar structure, and enhances sensitivity to PARP inhibitors and RNA Pol I inhibitors. RAD54L was identified as an unexpected protective factor in rDNA surveillance via a boutique CRISPR-Cas9 synthetic lethal screen. CRISPR-Cas9 synthetic lethal screen of DNA repair factors with RNA Pol I inhibitors, RAD54L knockout cells, R-loop quantification (DRIP assay), rDNA damage assays, nucleolar structure analysis by microscopy bioRxivpreprint Medium bio_10.1101_2025.01.20.633984
2025 RAD54L is required for the resolution of long RAD51/MND1-containing filamentous structures that form during homology search after DSB induction in living human cells. Loss of RAD54L prevented the resolution of these filaments, which are highly dynamic and explore nuclear space. This places RAD54L functionally downstream of RAD51 filament formation, at the step of homology search completion and strand invasion. Live-cell imaging with GFP-MND1 to visualize homology search filaments in human cells, RAD54L siRNA/knockout, time-lapse microscopy of filament dynamics and resolution bioRxivpreprint Medium bio_10.1101_2025.03.01.640932
2026 The transcription factor SOHLH2 transcriptionally activates RAD54L expression in non-small cell lung cancer. SOHLH2 overexpression promotes HR repair and radioresistance, while SOHLH2 knockdown suppresses these effects. Overexpression of RAD54L rescues the suppression of HR repair and radioresistance caused by SOHLH2 knockdown, establishing a SOHLH2→RAD54L transcriptional axis in NSCLC radioresistance. SOHLH2 knockdown and overexpression, RAD54L overexpression rescue experiments, chromatin immunoprecipitation (ChIP) for SOHLH2 binding to RAD54L promoter, HR repair assays, clonogenic survival after irradiation Cell death discovery Medium 41535248

Source papers

Stage 0 corpus · 58 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Cell 2861 17081983
1987 RNA splice junctions of different classes of eukaryotes: sequence statistics and functional implications in gene expression. Nucleic acids research 2261 3658675
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2011 DAXX/ATRX, MEN1, and mTOR pathway genes are frequently altered in pancreatic neuroendocrine tumors. Science (New York, N.Y.) 1392 21252315
2004 Large-scale characterization of HeLa cell nuclear phosphoproteins. Proceedings of the National Academy of Sciences of the United States of America 1159 15302935
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2010 Distinct factors control histone variant H3.3 localization at specific genomic regions. Cell 1038 20211137
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2005 Nucleolar proteome dynamics. Nature 934 15635413
2011 Altered telomeres in tumors with ATRX and DAXX mutations. Science (New York, N.Y.) 877 21719641
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2005 The DNA sequence of the human X chromosome. Nature 816 15772651
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2010 Daxx is an H3.3-specific histone chaperone and cooperates with ATRX in replication-independent chromatin assembly at telomeres. Proceedings of the National Academy of Sciences of the United States of America 674 20651253
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2010 The death-associated protein DAXX is a novel histone chaperone involved in the replication-independent deposition of H3.3. Genes & development 541 20504901
2012 Loss of ATRX, genome instability, and an altered DNA damage response are hallmarks of the alternative lengthening of telomeres pathway. PLoS genetics 508 22829774
1995 Mutations in a putative global transcriptional regulator cause X-linked mental retardation with alpha-thalassemia (ATR-X syndrome). Cell 494 7697714
2012 Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas. Oncotarget 463 22869205
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2000 Mutations in ATRX, encoding a SWI/SNF-like protein, cause diverse changes in the pattern of DNA methylation. Nature genetics 386 10742099
2012 Association of age at diagnosis and genetic mutations in patients with neuroblastoma. JAMA 351 22416102
2013 Loss of DAXX and ATRX are associated with chromosome instability and reduced survival of patients with pancreatic neuroendocrine tumors. Gastroenterology 348 24148618
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2010 ATRX interacts with H3.3 in maintaining telomere structural integrity in pluripotent embryonic stem cells. Genome research 338 20110566
2010 ATR-X syndrome protein targets tandem repeats and influences allele-specific expression in a size-dependent manner. Cell 337 21029860
2003 p53 interacts with hRAD51 and hRAD54, and directly modulates homologous recombination. Cancer research 143 12750285
2006 Single nucleotide polymorphisms of RecQ1, RAD54L, and ATM genes are associated with reduced survival of pancreatic cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 123 16520463
2015 Cross-Species Genomics Identifies TAF12, NFYC, and RAD54L as Choroid Plexus Carcinoma Oncogenes. Cancer cell 67 25965574
2021 Oct4 confers stemness and radioresistance to head and neck squamous cell carcinoma by regulating the homologous recombination factors PSMC3IP and RAD54L. Oncogene 39 34079088
1999 Search for mutations of the hRAD54 gene in sporadic meningiomas with deletion at 1p32. Molecular carcinogenesis 32 10326867
2020 E2F1 Promotes Progression of Bladder Cancer by Modulating RAD54L Involved in Homologous Recombination Repair. International journal of molecular sciences 31 33261027
2003 Implications of a RAD54L polymorphism (2290C/T) in human meningiomas as a risk factor and/or a genetic marker. BMC cancer 26 12614485
2022 RAD51AP1 and RAD54L Can Underpin Two Distinct RAD51-Dependent Routes of DNA Damage Repair via Homologous Recombination. Frontiers in cell and developmental biology 25 35652094
2001 Severe combined immunodeficient cells expressing mutant hRAD54 exhibit a marked DNA double-strand break repair and error-prone chromosome repair defect. Cancer research 25 11289143
2000 hRAD54 gene and 1p high-resolution deletion-mapping analyses in oligodendrogliomas. Cancer genetics and cytogenetics 25 10640146
2018 CDC7-dependent transcriptional regulation of RAD54L is essential for tumorigenicity and radio-resistance of glioblastoma. Translational oncology 16 29413763
2022 Rad54L promotes bladder cancer progression by regulating cell cycle and cell senescence. Medical oncology (Northwood, London, England) 14 36071250
2017 Serine/Threonine Kinase CHEK1-Dependent Transcriptional Regulation of RAD54L Promotes Proliferation and Radio Resistance in Glioblastoma. Translational oncology 13 29287241
2024 Disparate requirements for RAD54L in replication fork reversal. Nucleic acids research 12 39315725
2023 Pan-Cancer Analysis of Oncogenic Role of RAD54L and Experimental Validation in Hepatocellular Carcinoma. Journal of inflammation research 9 37719938
2008 Germline mutations in RAD51, RAD51AP1, RAD51B, RAD51C,RAD51D, RAD52 and RAD54L do not contribute to familial chronic lymphocytic leukemia. Leukemia & lymphoma 9 18203022
2023 RAD54L promotes progression of hepatocellular carcinoma via the homologous recombination repair pathway. Functional & integrative genomics 7 37071224
2021 Homologous recombination repair rathway and RAD54L in early-stage lung adenocarcinoma. PeerJ 7 33628633
2020 Germline RAD54L with somatic POLE defect implicated in Hypermutation phenotype: case report. BMC gastroenterology 6 32758138
2010 Relationship of an hRAD54 gene polymorphism (2290 C/T) in an Ecuadorian population with chronic myelogenous leukemia. Genetics and molecular biology 6 21637572
2005 Shortened telomeres in murine scid cells expressing mutant hRAD54 coincide with reduction in recombination at telomeres. Mutation research 5 15975611
2021 Association of MTHFR, MTRR and RAD54L Gene Variations with Meningioma and Correlation with Tumor's Histopathological Characteristics on Turkish Cohort. Turkish neurosurgery 3 34169999
2024 Disparate requirements for RAD54L in replication fork reversal. bioRxiv : the preprint server for biology 2 37546955
2025 Porcine reproductive and respiratory syndrome virus downregulates the circ-107191/miR-34c/RAD54L axis to promote testicular cell apoptosis via impaired homologous recombination repair. Theriogenology 1 40730084
2025 A Case of Metastatic Castration-Resistant Prostate Cancer With RAD54L Mutation Responding to Niraparib. IJU case reports 1 41185726
2024 Repeat expansion in a Fragile X model is independent of double strand break repair mediated by Pol θ, Rad52, Rad54l or Rad54b. bioRxiv : the preprint server for biology 1 39574643
2026 SOHLH2-RAD54L axis induces radioresistance by promoting homologous recombination repair in non-small cell lung cancer. Cell death discovery 0 41535248
2024 Novel Association of RAD54L Mutation with Müllerian Clear Cell Carcinoma of the Male Urethra: New Insights Regarding the Molecular Mechanisms of a Rare Tumour. Current cancer drug targets 0 38279717