ReviewCurrent opinion in genetics & development2021
RAD51 paralog function in replicative DNA damage and tolerance.
Review in Current opinion in genetics & development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 30 citations in OpenAlex.
- Spatiotemporal regulation of DNA repair proteins between Golgi and nucleus maintains genome stability.The Journal of cell biology · 2026Article
- A functional landscape for chromosome 17q in neuroblastoma: balancing replication stress and genomic stability.British journal of cancer · 2026Review
- Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Article
- Cancer mutations in RAD51 and its paralogues.PloS one · 2026Article
- Mechanism of Rad51 filament formation by Rad52 and Rad55-Rad57 in homologous recombination.Nature communications · 2025Article
- Comprehensive RAD51C ovarian cancer variant analysis uncouples homologous recombination and replicative functions.Nature communications · 2025Article
- The role of RAD51 regulators and variants in primary ovarian insufficiency, endometriosis, and polycystic ovary syndrome.NAR molecular medicine · 2024Review
- FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress.Nature communications · 2024Article
- Alternative splicing events driven by altered levels of GEMIN5 undergo translation.RNA biology · 2024Article
- HELQ as a DNA helicase: Its novel role in normal cell function and tumorigenesis (Review).Oncology reports · 2023Review
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
- Homologous Recombination Repair in Biliary Tract Cancers: A Prime Target for PARP Inhibition?Cancers · 2022Review
- Beyond BRCA1/2: Homologous Recombination Repair Genetic Profile in a Large Cohort of Apulian Ovarian Cancers.Cancers · 2022Article
- Homologous Recombination as a Fundamental Genome Surveillance Mechanism during DNA Replication.Genes · 2021Review
- Beyond base excision repair: an evolving picture of mitochondrial DNA repair.Bioscience reports · 2021Review
- RAD51 and RAD51 paralog inhibition sensitizes nonreplicating quiescent keratinocytes to UV radiation.Photochemistry and photobiologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
RAD51 paralog gene mutations are observed in both hereditary breast and ovarian cancers. Classically, defects in RAD51 paralog function are associated with homologous recombination (HR) deficiency and increased genomic instability. Several recent investigative advances have enabled characterization of non-canonical RAD51 paralog function during DNA replication. Here we discuss the role of the RAD51 paralogs and their associated complexes in integrating a robust response to DNA replication stress. We highlight recent discoveries suggesting that the RAD51 paralogs complexes mediate lesion-specific tolerance of replicative stress following exposure to alkylating agents and the requirement for the Shu complex in fork restart upon fork stalling by dNTP depletion. In addition, we describe the role of the BCDX2 complex in restraining and promoting fork remodeling in response to fluctuating dNTP pools. Finally, we highlight recent work demonstrating a requirement for RAD51C in recognizing and tolerating methyl-adducts. In each scenario, RAD51 paralog complexes play a central role in lesion recognition and bypass in a replicative context. Future studies will determine how these critical functions for RAD51 paralog complexes contribute to tumorigenesis.
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.