ArticleNucleic acids research2018
Increased levels of RECQ5 shift DNA repair from canonical to alternative pathways.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- Review
- Homologous recombination deficiency signatures in gastrointestinal and thoracic cancers correlate with platinum therapy duration.NPJ precision oncology · 2023Article
- Cas9/Nickase-induced allelic conversion by homologous chromosome-templated repair inScience advances · 2022Article
- Enzymatic Characterization of In Vitro Activity of RNA Methyltransferase PCIF1 on DNA.Biochemistry · 2022Article
- Pathways and signatures of mutagenesis at targeted DNA nicks.PLoS genetics · 2021Article
- Single-molecule visualization of human RECQ5 interactions with single-stranded DNA recombination intermediates.Nucleic acids research · 2021Article
- RECQL5 at theFrontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
RECQ5 (RECQL5) is one of several human helicases that dissociates RAD51-DNA filaments. The gene that encodes RECQ5 is frequently amplified in human tumors, but it is not known whether amplification correlates with increased gene expression, or how increased RECQ5 levels affect DNA repair at nicks and double-strand breaks. Here, we address these questions. We show that RECQ5 gene amplification correlates with increased gene expression in human tumors, by in silico analysis of over 9000 individual tumors representing 32 tumor types in the TCGA dataset. We demonstrate that, at double-strand breaks, increased RECQ5 levels inhibited canonical homology-directed repair (HDR) by double-stranded DNA donors, phenocopying the effect of BRCA deficiency. Conversely, at nicks, increased RECQ5 levels stimulated 'alternative' HDR by single-stranded DNA donors, which is normally suppressed by RAD51; this was accompanied by stimulation of mutagenic end-joining. Even modest changes (2-fold) in RECQ5 levels caused significant dysregulation of repair, especially HDR. These results suggest that in some tumors, RECQ5 gene amplification may have profound consequences for genomic instability.
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Registered trials
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