ArticleEMBO reports2017
RADX interacts with single-stranded DNA to promote replication fork stability.
Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 40 citations in OpenAlex.
- Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers.Scientific reports · 2026Article
- Distinct roles of RECQL5 in RAD51-mediated fork reversal and transcription elongation.Nucleic acids research · 2025Article
- Mechanisms and regulation of replication fork reversal.DNA repair · 2024Review
- Structure of RADX and mechanism for regulation of RAD51 nucleofilaments.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- ZNF827 is a single-stranded DNA binding protein that regulates the ATR-CHK1 DNA damage response pathway.Nature communications · 2024Article
- TFIP11 promotes replication fork reversal to preserve genome stability.Nature communications · 2024Article
- FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress.Nature communications · 2024Article
- Mechanisms of synthetic lethality between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta targeting.Nature communications · 2023Article
- CRISPR-dependent Base Editing Screens Identify Separation of Function Mutants of RADX with Altered RAD51 Regulatory Activity.Journal of molecular biology · 2023Article
- Structure of RADX and mechanism for regulation of RAD51 nucleofilaments.bioRxiv : the preprint server for biology · 2023Article
- Article
- Enzymatic Characterization of In Vitro Activity of RNA Methyltransferase PCIF1 on DNA.Biochemistry · 2022Article
- Article
- The comprehensive interactomes of human adenosine RNA methyltransferases and demethylases reveal distinct functional and regulatory features.Nucleic acids research · 2021Article
- Review
- RADX prevents genome instability by confining replication fork reversal to stalled forks.Molecular cell · 2021Article
- A fork in the road: Where homologous recombination and stalled replication fork protection part ways.Seminars in cell & developmental biology · 2021Review
- RADX controls RAD51 filament dynamics to regulate replication fork stability.Molecular cell · 2021Article
- Replication Fork Reversal and Protection.Frontiers in cell and developmental biology · 2021Review
- The plasticity of DNA replication forks in response to clinically relevant genotoxic stress.Nature reviews. Molecular cell 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single-stranded DNA (ssDNA) regions form as an intermediate in many DNA-associated transactions. Multiple cellular proteins interact with ssDNA via the oligonucleotide/oligosaccharide-binding (OB) fold domain. The heterotrimeric, multi-OB fold domain-containing Replication Protein A (RPA) complex has an essential genome maintenance role, protecting ssDNA regions from nucleolytic degradation and providing a recruitment platform for proteins involved in responses to replication stress and DNA damage. Here, we identify the uncharacterized protein RADX (CXorf57) as an ssDNA-binding factor in human cells. RADX binds ssDNA via an N-terminal OB fold cluster, which mediates its recruitment to sites of replication stress. Deregulation of RADX expression and ssDNA binding leads to enhanced replication fork stalling and degradation, and we provide evidence that a balanced interplay between RADX and RPA ssDNA-binding activities is critical for avoiding these defects. Our findings establish RADX as an important component of cellular pathways that promote DNA replication integrity under basal and stressful conditions by means of multiple ssDNA-binding proteins.
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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.