ReviewCell cycle (Georgetown, Tex.)2010
Helicase-inactivating mutations as a basis for dominant negative phenotypes.
Review in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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
23 citing papers in PubMed, 33 citations in OpenAlex.
- DNA binding contributes to dominant-negative effects of a catalytically inactive RecQ4-family helicase.Nucleic acids research · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Novel variants of the ATRX gene identified in MYCN non-amplified Neuroblastoma in Brazilian patients.Clinics (Sao Paulo, Brazil) · 2025Article
- WRN rescues replication forks compromised by a BRCA2 deficiency: Predictions for how inhibition of a helicase that suppresses premature aging tilts the balance to fork demise and chromosomal instability in cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Single-molecule studies of helicases and translocases in prokaryotic genome-maintenance pathways.DNA repair · 2021Review
- A deep dive into the RecQ interactome: something old and something new.Current genetics · 2021Review
- Modeling DNA trapping of anticancer therapeutic targets using missense mutations identifies dominant synthetic lethal interactions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Comprehensive Synthetic Genetic Array Analysis of Alleles That Interact with Mutation of theG3 (Bethesda, Md.) · 2020Article
- ATP-dependent helicase activity is dispensable for the physiological functions of Recql4.PLoS genetics · 2019Article
- Breast cancer patients suggestive of Li-Fraumeni syndrome: mutational spectrum, candidate genes, and unexplained heredity.Breast cancer research : BCR · 2018Article
- Small-Molecule Inhibitors Targeting DNA Repair and DNA Repair Deficiency in Research and Cancer Therapy.Cell chemical biology · 2017Review
- The Extraintestinal Pathogenic Escherichia coli Factor RqlI Constrains the Genotoxic Effects of the RecQ-Like Helicase RqlH.PLoS pathogens · 2015Article
- Insight into the roles of helicase motif Ia by characterizing Fanconi anemia group J protein (FANCJ) patient mutations.The Journal of biological chemistry · 2014Article
- Hrq1, a homolog of the human RecQ4 helicase, acts catalytically and structurally to promote genome integrity.Cell reports · 2014Article
- Molecular and cellular functions of the FANCJ DNA helicase defective in cancer and in Fanconi anemia.Frontiers in genetics · 2014Review
- The Gemin associates of survival motor neuron are required for motor function in Drosophila.PloS one · 2013Article
- The Q motif of Fanconi anemia group J protein (FANCJ) DNA helicase regulates its dimerization, DNA binding, and DNA repair function.The Journal of biological chemistry · 2012Article
- DNA helicase and helicase-nuclease enzymes with a conserved iron-sulfur cluster.Nucleic acids research · 2012Review
- Experimental approaches to identify cellular G-quadruplex structures and functions.Methods (San Diego, Calif.) · 2012Article
- Yin Yang 1 contains G-quadruplex structures in its promoter and 5'-UTR and its expression is modulated by G4 resolvase 1.Nucleic acids research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
There is ample evidence from studies of both unicellular and multicellular organisms that helicase-inactivating mutations lead to cellular dysfunction and disease phenotypes. In this review, we will discuss the mechanisms underlying the basis for abnormal phenotypes linked to mutations in genes encoding DNA helicases. Recent evidence demonstrates that a clinically relevant patient missense mutation in Fanconi Anemia Complementation Group J exerts detrimental effects on the biochemical activities of the FANCJ helicase, and these molecular defects are responsible for aberrant genomic stability and a poor DNA damage response. The ability of FANCJ to use the energy from ATP hydrolysis to produce the force required to unwind duplex or G-quadruplex DNA structures or destabilize protein bound to DNA is required for its DNA repair functions in vivo. Strikingly, helicase-inactivating mutations can exert a spectrum of dominant negative phenotypes, indicating that expression of the mutant helicase protein potentially interferes with normal DNA metabolism and has an effect on basic cellular processes such as DNA replication, the DNA damage response and protein trafficking. This review emphasizes that future studies of clinically relevant mutations in helicase genes will be important to understand the molecular pathologies of the associated diseases and their impact on heterozygote carriers.
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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.