Affinage

HELQ

Helicase POLQ-like · UniProt Q8TDG4

Length
1101 aa
Mass
124.1 kDa
Annotated
2026-04-28
42 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HELQ is a conserved 3′→5′ superfamily 2 DNA helicase that couples DNA unwinding with intrinsic strand annealing activity to maintain genome integrity at stalled replication forks and DNA double-strand breaks (PMID:34937945, PMID:21398521). Its N-terminal PWI-like domain mediates RPA-dependent recruitment to ssDNA substrates, where RAD51 paralogues (BCDX2 complex) stimulate translocation and unwinding while RPA suppresses unwinding but promotes annealing, enabling HELQ to participate in homologous recombination, single-strand annealing, microhomology-mediated end joining, synthesis-dependent strand annealing, and interstrand crosslink repair in parallel to the Fanconi anaemia pathway (PMID:24005329, PMID:34937945, PMID:34316696, PMID:24005041). HELQ additionally inhibits Pol δ–mediated DNA synthesis through a direct POLD3-binding intrinsically disordered region, promotes EXO1-dependent end resection, resolves R-loops in concert with XRN2, and suppresses ssDNA gap accumulation through a RAD52–BRCA axis (PMID:36718939, PMID:37897354, PMID:39965657, PMID:39530221). Helq-deficient mice exhibit subfertility, germ cell attrition, ICL hypersensitivity, and tumour predisposition, with germ cell defects linked to derepression of LINE-1 retrotransposons via dysregulated KDM4B-dependent H3K9me3 maintenance (PMID:24005329, PMID:40542648).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2005 Medium

    Establishing that the Hel308 family acts at stalled replication forks — archaeal Hel308 was shown to specifically displace lagging strands and D-loop invading strands, defining the substrate specificity of this helicase family for replication-associated structures.

    Evidence In vitro helicase assays with fork/D-loop substrates and in vivo synthetic lethality in E. coli stalled-fork strains

    PMID:15994460

    Open questions at the time
    • Archaeal system; relevance to mammalian HELQ not yet tested
    • No protein interaction partners identified
    • No structural information available
  2. 2007 High

    Determining the structural basis for Hel308 unwinding — the crystal structure revealed a five-domain architecture with domain V acting as an autoinhibitory 'molecular brake' that clamps extruded ssDNA, explaining how processivity is regulated.

    Evidence X-ray crystallography of archaeal Hel308, mutagenesis, streptavidin displacement and DNA unwinding assays

    PMID:17991488 PMID:18056710

    Open questions at the time
    • Structure solved for archaeal ortholog only
    • Mechanism of autoinhibition relief unknown
    • No co-crystal with DNA fork substrate
  3. 2010 Medium

    Identifying RPA as a physical partner that recruits Hel308 to ssDNA — archaeal Hel308 was found to bind RPA through a conserved C-terminal motif, suggesting a recruitment rather than direct stimulation mechanism.

    Evidence Pulldown assay, motif mutagenesis, helicase stimulation assay in archaeal system

    PMID:21195035

    Open questions at the time
    • Single pulldown without reciprocal validation
    • Interaction mapped in archaea, not yet confirmed for human HELQ
    • Functional consequence of recruitment not demonstrated in cells
  4. 2011 High

    Demonstrating that human HELQ localizes to damaged replication forks and preferentially unwinds lagging-strand DNA — this placed HELQ at the site of replication stress alongside RAD51 and FANCD2 in human cells.

    Evidence GFP-fusion live-cell imaging after camptothecin, helicase assays with fork-model substrates, RPA stimulation assay

    PMID:21398521

    Open questions at the time
    • Functional requirement at forks not tested by depletion
    • Mechanism of substrate strand selection unknown
  5. 2013 High

    Placing HELQ in a DNA repair pathway parallel to Fanconi anaemia — mouse knockouts and epistasis analyses revealed that HELQ interacts with the BCDX2 RAD51 paralogue complex, operates non-epistatically with FANCC, and contributes to ATR-CHK1 signaling during ICL repair, with Helq-deficient mice showing subfertility, germ cell loss, and tumour predisposition.

    Evidence Co-IP, MS interactome, mouse KO models (single and double mutants with FA genes), ICL sensitivity, phosphorylation assays, cytogenetic readouts

    PMID:24005041 PMID:24005329 PMID:24005565

    Open questions at the time
    • Direct biochemical mechanism of HELQ in ICL processing not resolved
    • How BCDX2 regulates HELQ enzymatically unknown
    • Tumour spectrum and penetrance not fully characterized
  6. 2017 Medium

    Defining the winged helix domain as a conserved duplex-DNA-binding module — mutagenesis showed that the WHD binds dsDNA and its interface with the RecA-like domain is essential for ATPase activity, a feature conserved from archaea to human HELQ.

    Evidence Isolated domain DNA binding assays, mutagenesis in archaeal and human HELQ, ATPase and helicase assays

    PMID:28738244

    Open questions at the time
    • No full-length human HELQ structure
    • How WHD-dsDNA binding coordinates with N-terminal RPA-loading domain unclear
  7. 2021 High

    Revealing HELQ's dual enzymatic nature — reconstitution showed that HELQ possesses intrinsic strand annealing activity alongside unwinding, with RAD51 stimulating unwinding and RPA switching the enzyme toward annealing, explaining HELQ's roles in SSA, MMEJ, and SDSA repair pathways.

    Evidence Biochemical reconstitution, single-molecule imaging, SSA/MMEJ/HR reporter assays in HELQ-deficient cells, PWI-like domain characterization

    PMID:34316696 PMID:34937945

    Open questions at the time
    • How the annealing-unwinding switch is structurally controlled unknown
    • In vivo stoichiometry of RAD51/RPA regulation of HELQ not determined
    • Contribution of dimerization to pathway choice unclear
  8. 2022 Medium

    Establishing HELQ as an early actor in synthesis-dependent strand annealing — Drosophila HELQ ortholog was shown to promote formation of recombination intermediates during SDSA, non-redundantly with BLM and FANCM helicases.

    Evidence Double-strand gap repair assay in Drosophila, genetic epistasis with blm and fancm

    PMID:35328029

    Open questions at the time
    • Precise step in SDSA where HELQ acts not biochemically defined
    • Conservation of this specific SDSA role in mammals not directly tested
  9. 2023 High

    Discovering that HELQ inhibits Pol δ and is reciprocally stimulated by POLD3 — a 70-amino-acid IDR of HELQ directly binds POLD3, halting DNA synthesis while POLD3 stimulates HELQ's strand annealing, establishing a regulatory handoff between DNA synthesis and annealing during repair.

    Evidence In vitro DNA synthesis inhibition assay, HELQ mutant mapping, Co-IP/pulldown of POLD3-HELQ, strand annealing assay

    PMID:36718939

    Open questions at the time
    • In vivo relevance of Pol δ inhibition not tested
    • Whether other replisome components modulate this interaction unknown
  10. 2023 High

    Separating HELQ's helicase and fork-protection functions — helicase activity was shown to be required for EXO1-mediated end resection, while ssDNA binding mediates fork recruitment and nascent DNA protection in synergy with CtIP, revealing separable structure-function contributions.

    Evidence HELQ-KO human cells, resection and fork protection assays, epistasis with CtIP/BRCA1/BRCA2, complementation with separation-of-function mutants

    PMID:37897354

    Open questions at the time
    • Structural basis for separable functions not resolved
    • How HELQ coordinates with EXO1 biochemically undefined
  11. 2023 High

    Identifying a catalytic switch controlling recombination — motif IVa in the RecA2 domain toggles between helicase and annealase modes; a single mutation caused 160,000-fold increased gene conversion, demonstrating that HELQ normally suppresses recombination in vivo.

    Evidence Site-directed mutagenesis, in vitro helicase/annealing assays, MD simulation, in vivo recombination assay in archaea

    PMID:37409572

    Open questions at the time
    • Whether motif IVa switch operates identically in human HELQ not tested
    • Structural basis for the conformational switch at atomic resolution unknown
  12. 2023 Medium

    Linking HELQ to mitotic DNA synthesis — HELQ was shown to be required at an early step for FANCD2-driven MiDAS at common fragile sites, placing HELQ downstream of FANCD2 mono-ubiquitination.

    Evidence HELQ-deficient cells, MiDAS assay, CFS stability assay, epistasis with FA components

    PMID:37777152

    Open questions at the time
    • Biochemical mechanism of HELQ at MiDAS not determined
    • Whether HELQ acts directly on CFS structures or indirectly through downstream effectors unclear
  13. 2024 Medium

    Defining a HELQ–RAD52–BRCA axis in ssDNA gap suppression — HELQ was found to specifically suppress cisplatin sensitivity caused by PRIMPOL overexpression by reducing ssDNA gap accumulation, with RAD52 promoting gaps through a BRCA-dependent mechanism.

    Evidence Genome-wide CRISPR KO screen, HELQ-KO cells, ssDNA gap assay, epistasis with RAD52 and BRCA

    PMID:39530221

    Open questions at the time
    • Biochemical mechanism by which HELQ fills or seals gaps unknown
    • Single-lab finding not independently replicated
  14. 2025 Medium

    Extending HELQ's substrate repertoire to R-loops — HELQ was shown to be recruited to R-loops via RPA and to resolve them in an ATPase-dependent manner, coordinating with XRN2 for RNA degradation, revealing a new non-DSB function.

    Evidence In-cell R-loop resolution assay, in vitro R-loop unwinding, Co-IP of HELQ–XRN2, catalytic mutant HELQ

    PMID:39965657

    Open questions at the time
    • In vivo significance for transcription-replication conflicts not tested
    • Single-lab finding, no independent replication
  15. 2025 Medium

    Uncovering a chromatin-regulatory role in germ cells — HELQ was found to interact with KDM4B, and its absence leads to derepression of LINE-1 retrotransposons via reduced H3K9me3, causing DNA damage and PGC proliferation failure reversible by retrotransposition inhibition.

    Evidence Co-IP of HELQ–KDM4B, H3K9me3 ChIP, LINE-1 expression assay, retrotransposition inhibitor rescue, mouse embryo HELQ-KO

    PMID:40542648

    Open questions at the time
    • Whether HELQ regulates KDM4B degradation or activity not distinguished
    • Generalizability beyond PGCs unclear
    • Single-lab Co-IP without reciprocal confirmation

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: (1) the atomic structure of full-length human HELQ, (2) the structural mechanism by which the annealing-unwinding switch is controlled in the mammalian enzyme, (3) the in vivo stoichiometry and regulation of the HELQ–RAD51/BCDX2–RPA tripartite complex, and (4) the biological significance of HELQ's Pol δ inhibition during repair in cells.
  • No full-length mammalian HELQ structure
  • Annealing-unwinding switch mechanism not structurally resolved
  • In vivo reconstitution of regulatory complexes lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 5 GO:0003677 DNA binding 4 GO:0140097 catalytic activity, acting on DNA 4
Localization
GO:0005634 nucleus 3 GO:0005694 chromosome 2
Pathway
R-HSA-73894 DNA Repair 6 R-HSA-69306 DNA Replication 3 R-HSA-1640170 Cell Cycle 2 R-HSA-1643685 Disease 2
Partners
KDM4BPOLD3RAD51BRAD51CRAD51DRPA1XRCC2XRN2
Complex memberships
HELQ–BCDX2 complex

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 HELQ directly interacts with the RAD51 paralogue complex BCDX2 and functions in parallel to the Fanconi anaemia pathway to promote efficient homologous recombination at damaged replication forks. Helq helicase-deficient mice exhibit subfertility, germ cell attrition, ICL sensitivity and tumour predisposition. Co-IP, mouse knockout model with defined phenotypic readouts (subfertility, ICL sensitivity, tumour predisposition), genetic epistasis with FA pathway Nature High 24005329
2013 Human HELQ is associated with the RAD51 paralogs RAD51B/C/D and XRCC2, and with the DNA damage-responsive kinase ATR. HELQ-knockout cells show reduced CHK1 phosphorylation after MMC treatment and reduced G2/M accumulation, placing HELQ in an ATR-CHK1 signaling arm during ICL repair. Proteomic/mass spectrometry interaction analysis, HELQ knockout cells, phosphorylation assay, cell cycle analysis after MMC treatment Nature communications High 24005565
2021 HELQ possesses both DNA unwinding and DNA strand annealing activities that are differentially regulated: RAD51 forms a complex with HELQ and strongly stimulates translocation/unwinding, whereas RPA inhibits DNA unwinding but strongly stimulates DNA strand annealing. HELQ can capture RPA-bound DNA strands and displace RPA to facilitate annealing of complementary sequences. HELQ deficiency compromises single-strand annealing (SSA) and microhomology-mediated end-joining (MMEJ) pathways and biases towards long-tract gene conversion during HR. Biochemical reconstitution in vitro, single-molecule imaging, HELQ-deficient cell lines with SSA/MMEJ/HR reporter assays, direct protein-protein interaction Nature High 34937945
2021 The non-catalytic N-terminal region of HelQ contains a PWI-like domain that mediates interaction with RPA, orchestrating loading of the helicase domains onto ssDNA. Once loaded, ATP-Mg2+ binding activates the helicase core, and HelQ translocates along ssDNA as a dimer. Domain characterization, in vitro binding assays, ATPase/helicase assays with mutant HelQ proteins, biochemical reconstitution NAR cancer High 34316696
2011 Human HEL308 localizes to damaged replication forks (colocalizing with RAD51 and FANCD2) upon camptothecin treatment, requires a 3' ssDNA overhang for loading, preferentially unwinds the lagging strand of stalled replication fork substrates, and its unwinding is stimulated by human RPA. GFP-fusion live cell imaging/colocalization, purified protein helicase assays with fork-model substrates, RPA stimulation assay The Journal of biological chemistry High 21398521
2008 C. elegans HEL-308 (HELQ ortholog) functions in ICL repair through a Fanconi anemia-dependent pathway, genetically distinct from the polq-1/BRCA1-dependent pathway, as established by epistasis analysis. Genetic epistasis analysis in C. elegans, survival assays, checkpoint/apoptosis readouts after ICL treatment DNA repair Medium 18472307
2013 Mouse HELQ is non-epistatic with FANCC: Helq/Fancc double-mutant mice display significantly worse phenotypes than either single mutant (chromosome instability, micronuclei, 53BP1 nuclear bodies), establishing that HELQ operates in a pathway distinct from the FA core complex for suppression of spontaneous replication-associated genome instability. Double-mutant mouse model, epistasis analysis, cytogenetic assays (micronuclei, 53BP1 bodies), FANCD2 ubiquitination assay Nucleic acids research High 24005041
2007 Crystal structure of archaeal Hel308 (HELQ homolog) reveals a five-domain architecture with a central pore lined with DNA-binding residues. Domain 5 acts as an autoinhibitory 'molecular brake' clamping ssDNA extruded through the pore to limit processivity. Hel308 can displace streptavidin from biotinylated DNA and partially displaces RPA/Alba1 but not RadA. X-ray crystallography, protein-streptavidin displacement assay, DNA unwinding assays with RPA/Alba1/RadA The Journal of biological chemistry High 18056710
2010 Archaeal Hel308 physically interacts with RPA via a conserved C-terminal amino acid motif; this interaction does not require SSB and is proposed to recruit Hel308 to aberrant ssDNA at blocked replication forks rather than directly stimulating helicase activity. Pulldown/interaction assay, motif mutagenesis, helicase stimulation assay DNA repair Medium 21195035
2007 Domain V (C-terminal) of archaeal Hel308 couples DNA binding to ATP hydrolysis and positions ssDNA relative to the helicase ratchet domain IV; mutagenesis of three arginine residues in domain V impairs DNA binding, unwinding, and ATPase activities. Site-directed mutagenesis, ATPase assay, helicase assay, DNA binding assay Journal of molecular biology Medium 17991488
2005 Archaeal Hel308 acts at stalled replication forks in vivo (synthetic lethality with E. coli dnaE stalled-fork strains) and in vitro specifically displaces lagging strands and the invading strand of D-loops. In vivo complementation/synthetic lethality assay, in vitro helicase assay with fork and D-loop substrates Nucleic acids research Medium 15994460
2023 Human HelQ halts DNA synthesis by Pol δ and by the Pol δ-PCNA-RPA holoenzyme; this inhibition maps to a 70-amino-acid intrinsically disordered region (IDR) of HelQ and is independent of HelQ DNA binding. The Pol δ subunit POLD3 physically interacts with HelQ via this IDR and strongly stimulates HelQ DNA strand annealing activity. In vitro DNA synthesis inhibition assay, HelQ mutant proteins, Co-IP/pulldown of POLD3-HelQ interaction, strand annealing assay Nucleic acids research High 36718939
2023 HELQ helicase activity is required for EXO1-mediated DSB end resection, while HELQ's ssDNA-binding capacity is required for its recruitment to stalled replication forks where it protects nascent DNA from degradation and prevents chromosome aberrations. HELQ synergizes with CtIP (but not BRCA1/BRCA2) in fork protection. HELQ-deficient human cells, resection assays, fork protection assay (nascent DNA degradation), epistasis with CtIP/BRCA1/BRCA2, genetic complementation with helicase-dead and ssDNA-binding mutants Nucleic acids research High 37897354
2023 In archaeal Hel308, motif IVa (F/YHHAGL) in the RecA2 domain acts as a catalytic switch that modulates both DNA helicase and strand annealing activities; a single substitution in motif IVa generates hyper-active helicase/annealase and causes 160,000-fold increased recombination (gene conversion only) in archaeal cells, revealing that Hel308 suppresses recombination in vivo. Site-directed mutagenesis, in vitro helicase/annealing assays, all-atom MD simulation, in vivo recombination assay in archaea Nucleic acids research High 37409572
2023 FANCD2-driven mitotic DNA synthesis (MiDAS) in untransformed human cells requires HELQ at an early step, with a prerequisite of FANCD2 mono-ubiquitination by FA proteins, and functions to preserve common fragile site (CFS) stability. HELQ-deficient cells, MiDAS assay, CFS stability assay, epistasis with FA pathway components Journal of molecular biology Medium 37777152
2022 In Drosophila, HELQ (MUS301 ortholog) promotes formation of recombination intermediates during synthesis-dependent strand annealing (SDSA), acting early in the process; double mutants of helq with blm or fancm show more severe SDSA defects than single mutants, indicating non-redundant roles. Double-strand gap repair assay in Drosophila, genetic epistasis (single and double mutants of helq, blm, fancm) Genes Medium 35328029
2025 Human HELQ is recruited to R-loops via RPA interaction through its N-terminal disordered domain; HELQ resolves R-loops in an ATPase/helicase-dependent manner and functionally interacts with the nuclear 5'→3' exoribonuclease XRN2 to coordinate R-loop unwinding with RNA degradation. In-cell R-loop resolution assay, in vitro R-loop unwinding, Co-IP of HELQ-XRN2 interaction, catalytic mutant HELQ Open biology Medium 39965657
2024 HELQ specifically suppresses cisplatin sensitivity in PRIMPOL-overexpressing cells by reducing ssDNA gap accumulation; RAD52 acts as a mediator that promotes ssDNA gap accumulation through a BRCA-dependent mechanism, defining a HELQ-RAD52-BRCA axis in ssDNA gap repair. CRISPR genome-wide KO screen, HELQ-KO cell lines, ssDNA gap accumulation assay, epistasis with RAD52 and BRCA Nucleic acids research Medium 39530221
2017 The winged helix domain (WHD) of archaeal Hel308 directly binds duplex DNA (but not ssDNA); mutations in a solvent-exposed α-helix reduce DNA binding and unwinding. The interface between WHD and a RecA-like domain is essential for ATPase and helicase activities. The isolated WHD of human HelQ also binds duplex DNA, indicating conservation. In vitro mutagenesis, DNA binding assays (isolated WHD vs. full-length), ATPase assay, helicase assay, interface disruption mutants DNA repair Medium 28738244
2025 HELQ interacts with the H3K9me3 demethylase KDM4B in primordial germ cells; absence of HELQ increases KDM4B protein levels, reduces H3K9me3 at LINE-1 retrotransposon loci, triggers LINE-1 expression and DNA damage accumulation, causing PGC proliferation defects reversible by retrotransposition inhibition. Co-IP of HELQ-KDM4B interaction, H3K9me3 ChIP, LINE-1 expression assay, retrotransposition inhibitor rescue, mouse embryo HELQ-KO FASEB journal Medium 40542648
2025 In C. elegans, HELQ (hel-308) contributes to ICL-induced deletion formation via end-joining, acting in parallel to POLQ-mediated end joining, as a mutagenic ICL repair mechanism distinct from translesion synthesis. C. elegans genetic knockout, whole-genome mutation spectrum analysis after psoralen ICL treatment Nature communications Medium 40082407

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Caenorhabditis elegans POLQ-1 and HEL-308 function in two distinct DNA interstrand cross-link repair pathways. DNA repair 86 18472307
2013 HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis. Nature 85 24005329
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
2009 Common design principles in the spliceosomal RNA helicase Brr2 and in the Hel308 DNA helicase. Molecular cell 75 19716790
2005 Archaeal Hel308 helicase targets replication forks in vivo and in vitro and unwinds lagging strands. Nucleic acids research 75 15994460
2013 Human DNA helicase HELQ participates in DNA interstrand crosslink tolerance with ATR and RAD51 paralogs. Nature communications 67 24005565
2021 HELQ is a dual-function DSB repair enzyme modulated by RPA and RAD51. Nature 58 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 33 24005041
2011 Human HEL308 localizes to damaged replication forks and unwinds lagging strand structures. The Journal of biological chemistry 33 21398521
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
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 17 34316696
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
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 Screening of HELQ in breast and ovarian cancer families. Familial cancer 8 26351136
2016 HELQ in cancer and reproduction. Neoplasma 8 27565320
2023 Interaction of human HelQ with DNA polymerase delta halts DNA synthesis and stimulates DNA single-strand annealing. Nucleic acids research 7 36718939
2021 Identification and Functional Investigation of Novel Heterozygous HELQ Mutations in Patients with Sertoli Cell-only Syndrome. Genetic testing and molecular biomarkers 7 34672775
2023 Human HELQ regulates DNA end resection at DNA double-strand breaks and stalled replication forks. Nucleic acids research 6 37897354
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
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
2025 HELQ upregulates PARP1 to drive platinum resistance and predict therapeutic response in ovarian cancer. Translational oncology 2 40381483
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 CRISPR knockout genome-wide screens identify the HELQ-RAD52 axis in regulating the repair of cisplatin-induced single-stranded DNA gaps. Nucleic acids research 2 39530221
2024 Helicase HELQ: Molecular Characters Fit for DSB Repair Function. International journal of molecular sciences 1 39201320
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