Affinage

HELQ

Helicase POLQ-like · UniProt Q8TDG4

Length
1101 aa
Mass
124.1 kDa
Annotated
2026-06-10
43 papers in source corpus 25 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HELQ is a conserved superfamily 2 DNA helicase that maintains genome stability at stalled replication forks and double-strand breaks by coupling DNA unwinding to homologous recombination and fork protection (PMID:24005329, PMID:24005565, PMID:42055550). Structural and biochemical work on the archaeal ortholog Hel308 established a five-domain helicase architecture in which a central pore lined with DNA-binding residues threads single-stranded DNA, a winged-helix domain couples duplex DNA binding to stimulate unwinding, and domain V plus a RecA2 motif IVa act as autoinhibitory 'molecular brakes' that tune both unwinding and strand-annealing output (PMID:18056710, PMID:28738244, PMID:37409572). The enzyme requires a 3' single-stranded overhang to load and preferentially displaces lagging strands at fork structures and the invading strands of D-loops (PMID:15994460, PMID:21398521); its N-terminal PWI-like domain mediates an RPA interaction that loads the helicase core onto RPA-coated ssDNA, after which it translocates as a dimer (PMID:34316696). HELQ is a dual-function enzyme whose helicase and DNA strand-annealing activities are antagonistically regulated: RPA inhibits unwinding but stimulates annealing, whereas RAD51 forms a complex with HELQ and stimulates translocation (PMID:34937945). Through direct interaction with the RAD51-paralogue BCDX2 complex it promotes homologous recombination and replication fork reversal, acting in parallel to the Fanconi anaemia pathway, and it additionally supports single-strand annealing and microhomology-mediated end-joining, regulates EXO1-dependent end resection, and inhibits Pol δ synthesis via an intrinsically disordered region that also binds POLD3 to stimulate annealing (PMID:24005329, PMID:24005041, PMID:34937945, PMID:36718939, PMID:37897354, PMID:42055550). Beyond fork and break repair, HELQ resolves R-loops in coordination with the exoribonuclease XRN2 and, in primordial germ cells, suppresses LINE-1 retrotransposition by interacting with the KDM4B demethylase to preserve H3K9me3 at LINE-1 loci (PMID:39965657, PMID:40542648). Helicase-deficient Helq mice show subfertility, germ cell attrition, interstrand crosslink sensitivity and tumour predisposition (PMID:24005329).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2005 High

    Established that the HELQ ortholog acts directly at stalled replication forks, defining its core biological target before its mechanism was understood.

    Evidence In vivo E. coli dnaE synthetic lethality and in vitro helicase assays on fork and D-loop substrates with archaeal Hel308

    PMID:15994460

    Open questions at the time
    • Archaeal system; human relevance not yet shown
    • Did not resolve loading or regulation
  2. 2007 High

    Resolved the structural basis of helicase action, showing a central DNA-binding pore and an autoinhibitory domain V brake that limits processivity.

    Evidence X-ray crystallography of S. solfataricus Hel308 with protein-displacement assays, plus domain V arginine mutagenesis with ATPase/unwinding assays

    PMID:17991488 PMID:18056710

    Open questions at the time
    • Archaeal protein
    • Physiological trigger releasing the brake not defined
  3. 2010 Medium

    Identified RPA as a physical partner that loads the helicase rather than driving its catalytic mechanism, addressing how the enzyme is recruited to ssDNA.

    Evidence Co-IP/pulldown with motif mapping and helicase stimulation assays on archaeal Hel308

    PMID:21195035

    Open questions at the time
    • Only modest (1.5-2x) stimulation
    • Archaeal C-terminal motif; human loading domain not yet mapped
  4. 2011 High

    Connected human HELQ to damaged forks in cells and reconstituted its substrate preference and RPA dependence, bridging archaeal mechanism to human biology.

    Evidence GFP live-cell imaging/co-localization with RAD51 and FANCD2 after camptothecin, plus in vitro helicase assays with human RPA

    PMID:21398521

    Open questions at the time
    • Co-localization does not prove direct partner interactions
    • Annealing activity not yet appreciated
  5. 2013 High

    Placed HELQ in homologous recombination via direct BCDX2/RAD51-paralogue binding and ATR-CHK1 signaling, acting in parallel to the Fanconi anaemia pathway.

    Evidence Reciprocal Co-IP, co-IP/MS interactome, mouse knockouts, FANCD2 ubiquitination, and double-mutant epistasis (Helq;Fancc) with ICL phenotypes

    PMID:24005041 PMID:24005329 PMID:24005565

    Open questions at the time
    • Molecular consequence of BCDX2 binding for unwinding not defined
    • Whether ATR effect is direct or downstream of recombination failure unclear
  6. 2017 High

    Defined the winged-helix domain as the module that couples duplex DNA binding to stimulate unwinding, refining the domain logic of the enzyme.

    Evidence WHD mutagenesis and isolated-domain DNA-binding/ATPase/helicase assays in Hel308 and human HelQ

    PMID:28738244

    Open questions at the time
    • WHD contribution in full-length human HELQ in cells not tested
  7. 2019 Medium

    Demonstrated sequence-dependent translocation kinetics at single-base resolution, revealing how DNA sequence modulates the ATP cycle.

    Evidence Single-molecule SPRNT nanopore tweezers on archaeal Hel308

    PMID:30649515

    Open questions at the time
    • Single lab, archaeal ortholog
    • Functional consequence in repair not addressed
  8. 2021 High

    Reframed HELQ as a dual-function enzyme whose unwinding and strand-annealing activities are antagonistically controlled by RPA and RAD51, and mapped the PWI-domain loading mechanism.

    Evidence Biochemical reconstitution, single-molecule imaging, and pathway-specific cell assays (SSA, MMEJ, gene conversion) plus domain mapping and dimeric translocation analysis

    PMID:34316696 PMID:34937945

    Open questions at the time
    • Switch between annealase and helicase modes in vivo not directly observed
    • Stoichiometry of the HELQ-RAD51 complex unresolved
  9. 2022 Medium

    Distinguished HELQ's early role in forming recombination intermediates from BLM's later processing during synthesis-dependent strand annealing.

    Evidence Drosophila double-strand gap repair assays with blm helq and helq fancm double mutants

    PMID:35328029

    Open questions at the time
    • Drosophila model
    • Molecular nature of the early intermediate not defined
  10. 2023 High

    Uncovered multiple non-canonical HELQ functions: a Pol δ-inhibiting/POLD3-binding intrinsically disordered region, control of EXO1 resection and fork protection with CtIP, a motif IVa catalytic switch, and a requirement in FANCD2-driven MiDAS.

    Evidence In vitro synthesis inhibition with domain-mapped mutants and POLD3 Co-IP; separation-of-function HELQ cells with resection/fiber/epistasis assays; motif IVa mutagenesis with MD simulations and archaeal recombination assay; MiDAS EdU assays

    PMID:36718939 PMID:37409572 PMID:37777152 PMID:37897354

    Open questions at the time
    • How these activities are coordinated on a single fork is unclear
    • MiDAS step placement inferred as 'early' without full mechanism
  11. 2024 Medium

    Extended HELQ function to ssDNA gap processing and end-joining-driven mutagenesis, defining a HELQ-RAD52-BRCA axis and a role in psoralen ICL deletion repair.

    Evidence Genome-wide CRISPR screens with PRIMPOL overexpression and epistasis (HELQ/RAD52/BRCA); C. elegans hel-308 mutant whole-genome sequencing of repair products

    PMID:39530221 PMID:40082407

    Open questions at the time
    • RAD52/BRCA axis placement partially inferential
    • Direct biochemical action on gaps not reconstituted
  12. 2025 High

    Demonstrated HELQ drives replication fork reversal with BCDX2 and broadened its scope to R-loop resolution with XRN2 and LINE-1 silencing via KDM4B/H3K9me3 in germ cells.

    Evidence DNA fiber, electron microscopy of reversed forks and reconstitution with leading-gap substrates; R-loop IF/in vitro resolution with catalytic-dead mutant and XRN2 Co-IP; Helq-KO PGCs with KDM4B Co-IP, H3K9me3 ChIP, and retrotransposition-inhibitor rescue

    PMID:39965657 PMID:40542648 PMID:42055550

    Open questions at the time
    • Whether fork reversal, R-loop, and chromatin functions share one mechanism or are independent is unknown
    • KDM4B regulation mechanism by HELQ undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How HELQ's helicase, annealase, fork-reversal, R-loop, and chromatin-silencing activities are partitioned and regulated across distinct genomic contexts in human cells remains unresolved.
  • No structure of human HELQ bound to BCDX2 or RAD51
  • No unified model integrating annealase and helicase mode-switching in vivo
  • Disease/clinical roles rest on Low-confidence expression-correlation studies

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 6 GO:0003677 DNA binding 4 GO:0140657 ATP-dependent activity 4 GO:0016787 hydrolase activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-73894 DNA Repair 5 R-HSA-69306 DNA Replication 3 R-HSA-1640170 Cell Cycle 2 R-HSA-8953854 Metabolism of RNA 1
Partners
BCDX2EXO1KDM4BPOLD3RAD51RPAXRN2
Complex memberships
BCDX2 (RAD51 paralogue complex)

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 Crystal structure of archaeal Hel308 (Sulfolobus solfataricus) reveals a five-domain architecture with a central pore lined with essential DNA-binding residues; domain V acts as an autoinhibitory 'molecular brake' that clamps single-stranded DNA extruded through the central pore, limiting helicase processivity. Hel308 can displace streptavidin from biotinylated DNA, and this protein-displacement activity is only partially inhibited by RPA or Alba1 pre-bound to DNA, while RadA pre-binding has no effect. X-ray crystallography (high-resolution crystal structure), in vitro helicase/protein-displacement assays The Journal of biological chemistry High 18056710
2007 Mutagenesis of three arginine residues in domain V of archaeal Hel308 demonstrates that domain V couples DNA binding to ATP hydrolysis and positions single-stranded DNA relative to the helicase ratchet domain IV for efficient fork unwinding. Site-directed mutagenesis, in vitro ATPase assay, DNA-binding and unwinding assays Journal of molecular biology High 17991488
2005 Archaeal Hel308 targets stalled replication forks in vivo (introduction into E. coli dnaE strains causes synthetic lethality, phenocopying RecQ) and in vitro specifically displaces lagging strands from fork structures; it also targets the invading strand of D-loops. In vivo genetic complementation (E. coli dnaE conditional lethality), in vitro helicase assays on replication fork and D-loop substrates Nucleic acids research High 15994460
2011 Human HEL308 (HELQ) localizes to damaged replication forks after camptothecin treatment, co-localizing with RAD51 and FANCD2. Purified HEL308 requires a 3′ single-stranded overhang to load onto DNA, preferentially unwinds the parental strands of a model stalled fork with a nascent lagging strand, and its unwinding activity is specifically stimulated by human RPA. GFP-tag live-cell imaging and co-localization, in vitro helicase assays with purified proteins, RPA stimulation assay The Journal of biological chemistry High 21398521
2010 Archaeal Hel308 physically interacts with RPA (but not SSB); interaction requires a conserved amino acid motif at the Hel308 C-terminus. RPA modestly stimulates Hel308 helicase activity (1.5–2 fold), supporting a model in which RPA loads Hel308 onto ssDNA at blocked replication forks rather than directly stimulating its unwinding mechanism. Co-immunoprecipitation / pulldown assays, deletion/mutation mapping, in vitro helicase stimulation assays DNA repair Medium 21195035
2013 HELQ directly interacts with the RAD51 paralogue complex BCDX2 and functions in parallel to the Fanconi anaemia pathway to promote homologous recombination at damaged replication forks. Helicase-deficient Helq mice show subfertility, germ cell attrition, ICL sensitivity and tumour predisposition. Co-immunoprecipitation (direct interaction with BCDX2), mouse knockout phenotyping, epistasis with FA pathway Nature High 24005329
2013 Human HELQ is associated with RAD51 paralogs RAD51B/C/D and XRCC2, and with the DNA damage-responsive kinase ATR, as revealed by proteomic analysis. HELQ knockout in human cells enhances sensitivity to mitomycin C and chromosome radial formation, and reduces CHK1 phosphorylation after MMC treatment, indicating HELQ participates in ATR-CHK1 signaling in response to ICL. Proteomic analysis (co-IP/MS), HELQ knockout in human cells, MMC sensitivity assay, immunoblot for CHK1 phosphorylation Nature communications High 24005565
2013 Helq acts in parallel (non-epistatic) to Fancc in suppressing spontaneous chromosome instability (micronuclei, 53BP1 nuclear bodies) and ICL sensitivity in mice; Helq-deficient cells have intact FANCD2 mono-ubiquitination and focus formation, placing HELQ outside the canonical FA core complex pathway. Mouse double mutant (Helqgt/gt; Fancc−/−) epistasis analysis, FANCD2 ubiquitination assay, cytogenetic analysis Nucleic acids research High 24005041
2017 The winged helix domain (WHD) of Hel308 promotes DNA binding and unwinding: mutations in a solvent-exposed α-helix of the WHD reduce DNA binding and unwinding. Isolated WHD binds duplex DNA but not ssDNA, and disrupting the interface between the WHD and the RecA-like domain abolishes ATPase and helicase activities. The isolated WHD of human HelQ also binds duplex DNA. Site-directed mutagenesis, in vitro DNA-binding assays, ATPase assay, helicase assay with isolated domain constructs DNA repair High 28738244
2019 Single-molecule nanopore tweezers (SPRNT) reveal that DNA bases at two specific sites within Hel308 control the kinetics of an ATP-independent step in the ATP hydrolysis cycle, demonstrating sequence-specific translocation kinetics during ssDNA translocation. Single-molecule SPRNT (picometer-resolution nanopore tweezers) Nucleic acids research Medium 30649515
2021 HELQ possesses both helicase and DNA strand annealing activities that are differentially regulated: RAD51 forms a complex with HELQ and strongly stimulates its translocation/unwinding activity, whereas RPA inhibits DNA unwinding but strongly stimulates DNA strand annealing. HELQ can capture RPA-bound ssDNA strands and displace RPA to facilitate annealing of complementary sequences. HELQ deficiency impairs single-strand annealing (SSA) and microhomology-mediated end-joining (MMEJ) pathways and biases towards long-tract gene conversion during homologous recombination. Biochemical reconstitution, single-molecule imaging, HELQ-deficient cell lines with specific pathway assays (SSA, MMEJ, gene conversion tract analysis) Nature High 34937945
2021 The N-terminal non-catalytic region of human HelQ contains a PWI-like domain that mediates interaction with RPA to orchestrate loading of HelQ helicase domains onto ssDNA. Once loaded, HelQ translocates along ssDNA as a dimer, activated by ATP-Mg2+ binding at the catalytic site. Specific HelQ-ssDNA interactions critical for the translocation mechanism were identified. Domain characterization with deletion constructs, RPA interaction assays (pulldown), in vitro helicase/translocation assays, mutagenesis of ssDNA contact residues NAR cancer High 34316696
2022 In Drosophila, HELQ, BLM, and FANCM helicases play distinct roles during synthesis-dependent strand annealing (SDSA): double mutants (blm helq and helq fancm) show more severe SDSA defects than single mutants, and HELQ and FANCM act early to promote formation of recombination intermediates that are then processed by BLM to prevent deletion-prone repair. Drosophila genetic double-strand gap repair assay, double mutant epistasis analysis Genes Medium 35328029
2023 Human HelQ halts DNA synthesis by DNA polymerase delta (Pol δ) and Pol δ-PCNA-RPA holoenzyme; this inhibition is independent of HelQ DNA binding and maps to a 70-amino-acid intrinsically disordered region of HelQ. POLD3 subunit of Pol δ physically interacts with HelQ via this intrinsically disordered region and strongly stimulates HelQ DNA strand annealing activity. HelQ cannot inhibit the isolated POLD1 catalytic subunit alone. In vitro DNA synthesis inhibition assays, novel HelQ mutant proteins, pulldown/Co-IP (POLD3-HelQ interaction), DNA strand annealing assays Nucleic acids research High 36718939
2023 HELQ helicase activity is required for EXO1-mediated DNA end resection at double-strand breaks (DSBs), while the ssDNA-binding capacity of HELQ is required for its recruitment to stalled replication forks, where it facilitates fork protection and prevents chromosome aberrations. HELQ synergizes with CtIP (but not BRCA1 or BRCA2) to protect stalled forks. HELQ knockout/mutant cells, resection assays (RPA/ssDNA accumulation), replication fork protection assays (DNA fiber), epistasis with CtIP/BRCA1/BRCA2, chromosome aberration analysis Nucleic acids research Medium 37897354
2023 A conserved motif IVa (F/YHHAGL) in the RecA2 domain of archaeal Hel308/HELQ acts as a catalytic switch modulating both DNA unwinding and strand annealing: a single amino acid substitution in motif IVa produces hyper-active helicase and annealase activities in vitro and causes a 160,000-fold increase in gene conversion (non-crossover) recombination in archaeal cells, while crossover recombination is unaffected. Site-directed mutagenesis, in vitro helicase and strand-annealing assays, all-atom molecular dynamics simulations, in vivo recombination assay in archaea Nucleic acids research High 37409572
2023 FANCD2-driven mitotic DNA synthesis (MiDAS) in untransformed human cells requires HELQ, which functions at an early step of this pathway; FANCD2 mono-ubiquitination by FA proteins is a prerequisite step upstream. HELQ-deficient cell analysis, MiDAS assay (EdU incorporation on metaphase chromosomes), genetic epistasis with FA pathway components Journal of molecular biology Medium 37777152
2024 In C. elegans, HELQ (hel-308) participates in end-joining during ICL repair, contributing to deletion formation at psoralen ICL sites; this is distinct from translesion synthesis-driven SNV formation mediated by POLH/REV1/3. C. elegans mutant analysis, whole-genome sequencing of repair products, epistasis with FA pathway (FANCD2, FANCI), TRAIP and FAN1 genetic analysis Nature communications Medium 40082407
2024 HELQ specifically suppresses cisplatin sensitivity caused by PRIMPOL-generated ssDNA gaps, with this suppression associated with reduced ssDNA accumulation. RAD52 acts as a mediator downstream; RAD52 promotes ssDNA gap accumulation through a BRCA-mediated mechanism, defining a HELQ–RAD52–BRCA axis in ssDNA gap processing. CRISPR genome-wide knockout screens, PRIMPOL-overexpression model, ssDNA accumulation assays, genetic epistasis (HELQ/RAD52/BRCA) Nucleic acids research Medium 39530221
2025 HELQ is recruited by RPA at R-loops and resolves R-loops in a manner dependent on its ATPase/helicase catalytic activity. HELQ functionally interacts with the nuclear 5'–3' exoribonuclease XRN2, coordinating R-loop unwinding (by HELQ) with RNA digestion (by XRN2). Cell-based R-loop assays (S9.6 immunofluorescence), in vitro R-loop resolution assay with purified proteins, co-IP (HELQ–XRN2 interaction), catalytic-dead HELQ mutant Open biology Medium 39965657
2025 HELQ interacts with the H3K9me3 demethylase KDM4B in primordial germ cells (PGCs); HELQ deficiency increases total and chromatin-bound KDM4B levels, reducing H3K9me3 at LINE-1 retrotransposon regions, which triggers LINE-1 expression and DNA damage accumulation in PGCs. Retrotransposition inhibition rescues the developmental defects of HELQ-deficient PGCs. Mouse Helq knockout, Co-IP (HELQ–KDM4B interaction), ChIP (H3K9me3 at LINE-1), retrotransposition inhibitor rescue experiment, PGC proliferation assays FASEB journal Medium 40542648
2025 HELQ promotes replication fork reversal: HELQ and BCDX2 act epistatically to slow replication fork progression under replication stress (DNA fiber assay), and electron microscopy shows that reversed fork structures are reduced in HELQ-knockout cells. Biochemical reconstitution demonstrates HELQ is stimulated by RPA on fork substrates containing a leading-strand gap. HELQ deletion suppresses nascent strand degradation when BRCA2- or FANCD2-dependent fork protection is lost. DNA fiber assay, electron microscopy of replication intermediates, biochemical reconstitution with fork substrates, HELQ-KO epistasis with BRCA2/FANCD2 Nucleic acids research High 42055550
2008 In C. elegans, hel-308 functions in ICL repair via a Fanconi anemia-dependent pathway, genetically distinct from polq-1/POLQ which operates through a brc-1 (CeBRCA1)-dependent pathway; epistatic and cytological analyses establish these as parallel mechanisms. C. elegans mutant survival assays, checkpoint/apoptosis cytology, genetic epistasis (hel-308 vs. FA pathway vs. polq-1/brc-1) DNA repair Medium 18472307
2016 HELQ overexpression or knockdown in osteosarcoma cells alters expression of CHK1 and RAD51 proteins, with HELQ overexpression increasing CHK1 and RAD51 levels and reducing invasion/migration, while knockdown has the opposite effects. The antitumor activities of HELQ are associated with upregulation of CHK1-RAD51 signaling. shRNA knockdown and lentiviral overexpression, western blot, Transwell invasion, wound healing, Comet assay Oncology reports Low 28000895
2025 HELQ promotes OC platinum resistance by upregulating PARP1 expression; HELQ overexpression increases PARP1 levels, and PARP1 downregulation reverses the HELQ-mediated resistance. HELQ overexpression also sensitizes OC cells to PARP inhibitors. HELQ overexpression/knockdown in cell lines, western blot (PARP1, γH2AX, RPA1, 53BP1), PARP1 knockdown rescue, CCK8 viability assay, in vivo xenograft Translational oncology Low 40381483

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis. Nature 87 24005329
2008 Caenorhabditis elegans POLQ-1 and HEL-308 function in two distinct DNA interstrand cross-link repair pathways. DNA repair 86 18472307
2009 Structural evidence for consecutive Hel308-like modules in the spliceosomal ATPase Brr2. Nature structural & molecular biology 82 19525970
2007 Structure of the DNA repair helicase hel308 reveals DNA binding and autoinhibitory domains. The Journal of biological chemistry 82 18056710
2005 Archaeal Hel308 helicase targets replication forks in vivo and in vitro and unwinds lagging strands. Nucleic acids research 76 15994460
2009 Common design principles in the spliceosomal RNA helicase Brr2 and in the Hel308 DNA helicase. Molecular cell 75 19716790
2013 Human DNA helicase HELQ participates in DNA interstrand crosslink tolerance with ATR and RAD51 paralogs. Nature communications 69 24005565
2021 HELQ is a dual-function DSB repair enzyme modulated by RPA and RAD51. Nature 59 34937945
2019 Determining the effects of DNA sequence on Hel308 helicase translocation along single-stranded DNA using nanopore tweezers. Nucleic acids research 34 30649515
2013 Helq acts in parallel to Fancc to suppress replication-associated genome instability. Nucleic acids research 34 24005041
2011 Human HEL308 localizes to damaged replication forks and unwinds lagging strand structures. The Journal of biological chemistry 34 21398521
2021 The HelQ human DNA repair helicase utilizes a PWI-like domain for DNA loading through interaction with RPA, triggering DNA unwinding by the HelQ helicase core. NAR cancer 18 34316696
2010 Physical interaction between archaeal DNA repair helicase Hel308 and Replication Protein A (RPA). DNA repair 18 21195035
2007 Archaeal Hel308 domain V couples DNA binding to ATP hydrolysis and positions DNA for unwinding over the helicase ratchet. Journal of molecular biology 18 17991488
2018 Helicase POLQ-like (HELQ) as a novel indicator of platinum-based chemoresistance for epithelial ovarian cancer. Gynecologic oncology 16 29572031
2011 Winged helix domains with unknown function in Hel308 and related helicases. Biochemical Society transactions 14 21265761
2017 DNA binding and unwinding by Hel308 helicase requires dual functions of a winged helix domain. DNA repair 13 28738244
2016 HELQ reverses the malignant phenotype of osteosarcoma cells via CHK1-RAD51 signaling pathway. Oncology reports 11 28000895
2023 HELQ as a DNA helicase: Its novel role in normal cell function and tumorigenesis (Review). Oncology reports 10 37921071
2016 Screening of HELQ in breast and ovarian cancer families. Familial cancer 9 26351136
2023 Interaction of human HelQ with DNA polymerase delta halts DNA synthesis and stimulates DNA single-strand annealing. Nucleic acids research 8 36718939
2023 Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ. Journal of molecular biology 8 37777152
2022 Division of Labor by the HELQ, BLM, and FANCM Helicases during Homologous Recombination Repair in Drosophila melanogaster. Genes 8 35328029
2016 HELQ in cancer and reproduction. Neoplasma 8 27565320
2023 Human HELQ regulates DNA end resection at DNA double-strand breaks and stalled replication forks. Nucleic acids research 7 37897354
2021 Identification and Functional Investigation of Novel Heterozygous HELQ Mutations in Patients with Sertoli Cell-only Syndrome. Genetic testing and molecular biomarkers 7 34672775
2016 Structure-function analysis of DNA helicase HELQ: A new diagnostic marker in ovarian cancer. Oncology letters 6 28101207
2023 Archaeal Hel308 suppresses recombination through a catalytic switch that controls DNA annealing. Nucleic acids research 5 37409572
2015 The screening of HELQ gene in Chinese patients with premature ovarian failure. Reproductive biomedicine online 5 26190809
2024 Evolutionary and functional insights into the Ski2-like helicase family in Archaea: a comparison of Thermococcales ASH-Ski2 and Hel308 activities. NAR genomics and bioinformatics 4 38500564
2022 HELQ suppresses migration and proliferation of non-small cell lung cancer cells by repairing DNA damage and inducing necrosis. Cell biology international 4 36183369
2025 FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations. Nature communications 3 40082407
2025 HELQ upregulates PARP1 to drive platinum resistance and predict therapeutic response in ovarian cancer. Translational oncology 3 40381483
2024 CRISPR knockout genome-wide screens identify the HELQ-RAD52 axis in regulating the repair of cisplatin-induced single-stranded DNA gaps. Nucleic acids research 3 39530221
2020 [Expressions of HELQ and RAD51C in endometrial stromal sarcoma and their clinical significance]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 3 32895148
2025 The human HELQ helicase and XRN2 exoribonuclease cooperate in R-loop resolution. Open biology 2 39965657
2024 CRISPR knockout genome-wide screens identify the HELQ-RAD52 axis in regulating the repair of cisplatin-induced single stranded DNA gaps. bioRxiv : the preprint server for biology 2 38659927
2024 Helicase HELQ: Molecular Characters Fit for DSB Repair Function. International journal of molecular sciences 1 39201320
2026 The DNA helicase HELQ promotes replication fork reversal in coordination with BRCA2- and FANCD2-mediated repair pathways. Nucleic acids research 0 42055550
2025 Correction to "HELQ deficiency impairs the induction of primordial germ cell-like cells". FEBS open bio 0 40176377
2025 HELQ Maintains Genome Stability of Primordial Germ Cells by Inhibiting LINE-1 Expression. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 40542648
2024 A Human Homozygous HELQ Missense Variant Does Not Cause Premature Ovarian Insufficiency in a Mouse Model. Genes 0 38540391
2024 HELQ deficiency impairs the induction of primordial germ cell-like cells. FEBS open bio 0 38720471

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