ArticleNature communications2019
SPRTN protease and checkpoint kinase 1 cross-activation loop safeguards DNA replication.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- A CHK1-mediated phosphorylation switch suppresses human Topoisomerase 1-associated genomic instability.The EMBO journal · 2026Article
- Ubiquitin's code: UPS orchestrating DNA repair and genomic stability under genotoxic stress.Molecular and cellular biochemistry · 2026Review
- ACRC/GCNA is an essential protease that repairs DNA-protein crosslinks during vertebrate development.Nucleic acids research · 2026Article
- Living Cells Employ Ubiquitin-Proteasomal System and Nucleotide Excision Repair Pathways to Remove Reactive Oxygen Species-Induced DNA-Protein Crosslinks (ROS-DPCs).bioRxiv : the preprint server for biology · 2026Article
- SPRTN preserves RNA polymerase I transcription under genotoxic drug stress in lung adenocarcinoma.Frontiers in oncology · 2026Article
- The dual ubiquitin binding mode of SPRTN secures rapid spatiotemporal proteolysis of DNA-protein crosslinks.Nucleic acids research · 2025Article
- The cullin Rtt101 promotes ubiquitin-dependent DNA-protein crosslink repair across the cell cycle.Nucleic acids research · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Aldehyde-mediated inhibition of asparagine biosynthesis has implications for diabetes and alcoholism.Chemical science · 2024Article
- Isolation and detection of DNA-protein crosslinks in mammalian cells.Nucleic acids research · 2024Article
- Article
- Self-reversal facilitates the resolution of HMCES DNA-protein crosslinks in cells.Cell reports · 2023Article
- SPRTN-dependent DPC degradation precedes repair of damaged DNA: a proof of concept revealed by the STAR assay.Nucleic acids research · 2023Article
- Contribution of proteases to the hallmarks of aging and to age-related neurodegeneration.Aging cell · 2022Review
- USP1-trapping lesions as a source of DNA replication stress and genomic instability.Nature communications · 2022Article
- Targeting DNA-Protein CrosslinksFrontiers in molecular biosciences · 2022Review
- TEX264 at the intersection of autophagy and DNA repair.Autophagy · 2022Review
- Mechanisms and Regulation of DNA-Protein Crosslink Repair During DNA Replication by SPRTN Protease.Frontiers in molecular biosciences · 2022Review
- Immunofluorescence microscopy-based detection of ssDNA foci by BrdU in mammalian cells.STAR protocols · 2021Article
- The protease SPRTN and SUMOylation coordinate DNA-protein crosslink repair to prevent genome instability.Cell reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
The SPRTN metalloprotease is essential for DNA-protein crosslink (DPC) repair and DNA replication in vertebrate cells. Cells deficient in SPRTN protease exhibit DPC-induced replication stress and genome instability, manifesting as premature ageing and liver cancer. Here, we provide a body of evidence suggesting that SPRTN activates the ATR-CHK1 phosphorylation signalling cascade during physiological DNA replication by proteolysis-dependent eviction of CHK1 from replicative chromatin. During this process, SPRTN proteolyses the C-terminal/inhibitory part of CHK1, liberating N-terminal CHK1 kinase active fragments. Simultaneously, CHK1 full length and its N-terminal fragments phosphorylate SPRTN at the C-terminal regulatory domain, which stimulates SPRTN recruitment to chromatin to promote unperturbed DNA replication fork progression and DPC repair. Our data suggest that a SPRTN-CHK1 cross-activation loop plays a part in DNA replication and protection from DNA replication stress. Finally, our results with purified components of this pathway further support the proposed model of a SPRTN-CHK1 cross-activation loop.
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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.