ArticleNucleic acids research2013
Helq acts in parallel to Fancc to suppress replication-associated genome instability.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- HELQ & Hel308: ancient enzymes of DNA repair and recombination.Biochemical Society transactions · 2026Review
- The DNA helicase HELQ promotes replication fork reversal in coordination with BRCA2- and FANCD2-mediated repair pathways.Nucleic acids research · 2026Article
- 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
- Helicase HELQ: Molecular Characters Fit for DSB Repair Function.International journal of molecular sciences · 2024Review
- HELQ deficiency impairs the induction of primordial germ cell-like cells.FEBS open bio · 2024Article
- A Human HomozygousGenes · 2024Article
- FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress.Nature communications · 2024Article
- Human HELQ regulates DNA end resection at DNA double-strand breaks and stalled replication forks.Nucleic acids research · 2023Article
- 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
- Interaction of human HelQ with DNA polymerase delta halts DNA synthesis and stimulates DNA single-strand annealing.Nucleic acids research · 2023Article
- Review
- Helicase Q promotes homology-driven DNA double-strand break repair and prevents tandem duplications.Nature communications · 2021Article
- Cell-fate transition and determination analysis of mouse male germ cells throughout development.Nature communications · 2021Article
- Article
- Review
- Control of homologous recombination by the HROB-MCM8-MCM9 pathway.Genes & development · 2019Article
- Mitotic DNA Synthesis Is Differentially Regulated between Cancer and Noncancerous Cells.Molecular cancer research : MCR · 2019Article
- Around and beyond 53BP1 Nuclear Bodies.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
HELQ is a superfamily 2 DNA helicase found in archaea and metazoans. It has been implicated in processing stalled replication forks and in repairing DNA double-strand breaks and inter-strand crosslinks. Though previous studies have suggested the possibility that HELQ is involved in the Fanconi anemia (FA) pathway, a dominant mechanism for inter-strand crosslink repair in vertebrates, this connection remains elusive. Here, we investigated this question in mice using the Helq(gt) and Fancc(-) strains. Compared with Fancc(-)(/)(-) mice lacking FANCC, a component of the FA core complex, Helq(gt/gt) mice exhibited a mild of form of FA-like phenotypes including hypogonadism and cellular sensitivity to the crosslinker mitomycin C. However, unlike Fancc(-)(/)(-) primary fibroblasts, Helq(gt/gt) cells had intact FANCD2 mono-ubiquitination and focus formation. Notably, for all traits examined, Helq was non-epistatic with Fancc, as Helq(gt)(/gt);Fancc(-)(/)(-) double mutants displayed significantly worsened phenotypes than either single mutant. Importantly, this was most noticeable for the suppression of spontaneous chromosome instability such as micronuclei and 53BP1 nuclear bodies, known consequences of persistently stalled replication forks. These findings suggest that mammalian HELQ contributes to genome stability in unchallenged conditions through a mechanism distinct from the function of FANCC.
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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.