ArticleNature communications2021
Helicase Q promotes homology-driven DNA double-strand break repair and prevents tandem duplications.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 31 citations in OpenAlex.
- HELQ & Hel308: ancient enzymes of DNA repair and recombination.Biochemical Society transactions · 2026Review
- Interfering with DNA repair pathways to enhance CRISPR-Cas9-mediated homology-directed repair in a chelicerate genetic model.iScience · 2026Article
- Optimizing microhomology-based genome editing by engineering DNA polymerase θ for improved efficiency and reduced on-target indels.Cell reports methods · 2026Article
- A mutational scar-based genome-wide map of DNA double-strand break repair.Nature communications · 2026Article
- The DNA helicase HELQ promotes replication fork reversal in coordination with BRCA2- and FANCD2-mediated repair pathways.Nucleic acids research · 2026Article
- TONSL suppresses polymerase theta-dependent tandem duplications through chromatin-guided repair.Nature communications · 2026Article
- Decoding the Avian Missing Gene Mystery: Dot Chromosomes Unmask Extensive Gene Loss and Novel Genetic Instability.Genome biology and evolution · 2026Article
- Beyond Short Microhomologies: Mismatch-Compatible Pol θ-Mediated DNA Damage Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Diversity at the HYP1 locus in potato cyst nematodes does not result from developmentally-programmed somatic mutations.PloS one · 2026Article
- Review
- HELQ upregulates PARP1 to drive platinum resistance and predict therapeutic response in ovarian cancer.Translational oncology · 2025Article
- 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 · 2025Article
- Division of labor within polymerase theta in repair of CRISPR-induced DNA breaks inPNAS nexus · 2025Article
- FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations.Nature communications · 2025Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Microhomology-Mediated End-Joining Chronicles: Tracing the Evolutionary Footprints of Genome Protection.Annual review of cell and developmental biology · 2024Review
- Helicase HELQ: Molecular Characters Fit for DSB Repair Function.International journal of molecular sciences · 2024Review
- Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?Cells · 2024Review
- HELQ as a DNA helicase: Its novel role in normal cell function and tumorigenesis (Review).Oncology reports · 2023Review
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
DNA double-strand breaks are a major threat to cellular survival and genetic integrity. In addition to high fidelity repair, three intrinsically mutagenic DNA break repair routes have been described, i.e. single-strand annealing (SSA), polymerase theta-mediated end-joining (TMEJ) and residual ill-defined microhomology-mediated end-joining (MMEJ) activity. Here, we identify C. elegans Helicase Q (HELQ-1) as being essential for MMEJ as well as for SSA. We also find HELQ-1 to be crucial for the synthesis-dependent strand annealing (SDSA) mode of homologous recombination (HR). Loss of HELQ-1 leads to increased genome instability: patchwork insertions arise at deletion junctions due to abortive rounds of polymerase theta activity, and tandem duplications spontaneously accumulate in genomes of helq-1 mutant animals as a result of TMEJ of abrogated HR intermediates. Our work thus implicates HELQ activity for all DSB repair modes guided by complementary base pairs and provides mechanistic insight into mutational signatures common in HR-defective cancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.