ArticleMolecular cell2018
Removal of RTF2 from Stalled Replisomes Promotes Maintenance of Genome Integrity.
Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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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.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- RTF2 and CLASPIN localize CHK1 to the replication fork to control S-phase progression.Science advances · 2026Article
- ACRC/GCNA is an essential protease that repairs DNA-protein crosslinks during vertebrate development.Nucleic acids research · 2026Article
- Nrf1 acts as a highly-conserved determinon for maintaining robust redox homeostasis in the eco-evo-devo process of life histories.Cell stress · 2025Review
- Article
- Variant-to-function mapping of late-onset Alzheimer's disease GWAS signals in human microglial cell models implicatesbioRxiv : the preprint server for biology · 2024Article
- Improved detection of DNA replication fork-associated proteins.Cell reports · 2024Article
- The SPATA5-SPATA5L1 ATPase complex directs replisome proteostasis to ensure genome integrity.Cell · 2024Article
- Article
- Domains in Action: Understanding Ddi1's Diverse Functions in the Ubiquitin-Proteasome System.International journal of molecular sciences · 2024Review
- RTF2 controls replication repriming and ribonucleotide excision at the replisome.Nature communications · 2024Article
- Isolation and detection of DNA-protein crosslinks in mammalian cells.Nucleic acids research · 2024Article
- Aldehyde-induced DNA-protein crosslinks- DNA damage, repair and mutagenesis.Frontiers in oncology · 2024Review
- Early recovery of proteasome activity in cells pulse-treated with proteasome inhibitors is independent of DDI2.bioRxiv : the preprint server for biology · 2023Article
- Extended lifespan and improved genome stability in HepaRG-derived cell lines through reprogramming by high-density stress.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- DDI2 promotes tumor metastasis and resists antineoplastic drugs-induced apoptosis in colorectal cancer.Apoptosis : an international journal on programmed cell death · 2023Article
- Changes in hemoglobin oxidation and band 3 during blood storage impact oxygen sensing and mitochondrial bioenergetic pathways in the human pulmonary arterial endothelial cell model.Frontiers in physiology · 2023Article
- Article
- Mammalian Ddi2 is a shuttling factor containing a retroviral protease domain that influences binding of ubiquitylated proteins and proteasomal degradation.The Journal of biological chemistry · 2022Article
- Transcription of the Envelope Protein by 1-L Protein-RNA Recognition Code Leads to Genes/Proteins That Are Relevant to the SARS-CoV-2 Life Cycle and Pathogenesis.Current issues in molecular biology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The protection and efficient restart of stalled replication forks is critical for the maintenance of genome integrity. Here, we identify a regulatory pathway that promotes stalled forks recovery from replication stress. We show that the mammalian replisome component C20orf43/RTF2 (homologous to S. pombe Rtf2) must be removed for fork restart to be optimal. We further show that the proteasomal shuttle proteins DDI1 and DDI2 are required for RTF2 removal from stalled forks. Persistence of RTF2 at stalled forks results in fork restart defects, hyperactivation of the DNA damage signal, accumulation of single-stranded DNA (ssDNA), sensitivity to replication drugs, and chromosome instability. These results establish that RTF2 removal is a key determinant for the ability of cells to manage replication stress and maintain genome integrity.
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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.