ArticleNucleic acids research2012
Characterization of human Spartan/C1orf124, an ubiquitin-PCNA interacting regulator of DNA damage tolerance.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- The other side of the coin: protein deubiquitination by Ubiquitin-Specific Protease 1 in cancer progression and therapy.Future medicinal chemistry · 2025Review
- Quantification of Intracellular DNA-Protein Cross-Links with N7-Methyl-2'-Deoxyguanosine and Their Contribution to Cytotoxicity.Chemical research in toxicology · 2024Article
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health.Molecular and cellular biology · 2023Article
- A series of xanthenes inhibiting Rad6 function and Rad6-Rad18 interaction in the PCNA ubiquitination cascade.iScience · 2022Article
- Participation of Histones in DNA Damage and Repair within Nucleosome Core Particles: Mechanism and Applications.Accounts of chemical research · 2022Article
- USP1-trapping lesions as a source of DNA replication stress and genomic instability.Nature communications · 2022Article
- Cleavage-defective Topoisomerase I mutants sharply increase G-quadruplex-associated genomic instability.Microbial cell (Graz, Austria) · 2022Article
- Mechanisms and Regulation of DNA-Protein Crosslink Repair During DNA Replication by SPRTN Protease.Frontiers in molecular biosciences · 2022Review
- The protease SPRTN and SUMOylation coordinate DNA-protein crosslink repair to prevent genome instability.Cell reports · 2021Article
- Translesion Synthesis or Repair by Specialized DNA Polymerases Limits Excessive Genomic Instability upon Replication Stress.International journal of molecular sciences · 2021Review
- Mechanisms of damage tolerance and repair during DNA replication.Nucleic acids research · 2021Review
- DNA-protein crosslink proteases in genome stability.Communications biology · 2021Review
- DNA Damage Tolerance Pathways in Human Cells: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
- Debulking of topoisomerase DNA-protein crosslinks (TOP-DPC) by the proteasome, non-proteasomal and non-proteolytic pathways.DNA repair · 2020Review
- DNA-protein crosslinks from environmental exposure: Mechanisms of formation and repair.Environmental and molecular mutagenesis · 2020Review
- Robust high-throughput assays to assess discrete steps in ubiquitination and related cascades.BMC molecular and cell biology · 2020Article
- GCNA Interacts with Spartan and Topoisomerase II to Regulate Genome Stability.Developmental cell · 2020Article
- DNA-protein cross-link repair: what do we know now?Cell & bioscience · 2020Review
- Multilevel structure-activity profiling reveals multiple green tea compound families that each modulate ubiquitin-activating enzyme and ubiquitination by a distinct mechanism.Scientific reports · 2019Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Unrepaired DNA damage may arrest ongoing replication forks, potentially resulting in fork collapse, increased mutagenesis and genomic instability. Replication through DNA lesions depends on mono- and polyubiquitylation of proliferating cell nuclear antigen (PCNA), which enable translesion synthesis (TLS) and template switching, respectively. A proper replication fork rescue is ensured by the dynamic ubiquitylation and deubiquitylation of PCNA; however, as yet, little is known about its regulation. Here, we show that human Spartan/C1orf124 protein provides a higher cellular level of ubiquitylated-PCNA by which it regulates the choice of DNA damage tolerance pathways. We find that Spartan is recruited to sites of replication stress, a process that depends on its PCNA- and ubiquitin-interacting domains and the RAD18 PCNA ubiquitin ligase. Preferential association of Spartan with ubiquitin-modified PCNA protects against PCNA deubiquitylation by ubiquitin-specific protease 1 and facilitates the access of a TLS polymerase to the replication fork. In concert, depletion of Spartan leads to increased sensitivity to DNA damaging agents and causes elevated levels of sister chromatid exchanges. We propose that Spartan promotes genomic stability by regulating the choice of rescue of stalled replication fork, whose mechanism includes its interaction with ubiquitin-conjugated PCNA and protection against PCNA deubiquitylation.
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Registered trials
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