ArticleThe Journal of biological chemistry2012
DNA polymerase δ and ζ switch by sharing accessory subunits of DNA polymerase δ.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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
120 citing papers in PubMed, 156 citations in OpenAlex.
- Docking-Based Virtual Screening Identifies a Small-Molecule Inhibitor of the Translesion Synthesis REV7/REV3 Protein-Protein Interaction.ChemMedChem · 2026Article
- TASP1-mediated cleavage of REV3L enhances the activity of DNA polymerase ζ in mammalian cells.Nature communications · 2026Article
- Opposing regulation by Rev1 of DNA polymerase zeta activity on damaged versus undamaged DNA.Nucleic acids research · 2026Article
- Iron-sulfur cofactors in nucleic acid metabolism and protein synthesis: Assembly, delivery, and putative roles in cellular and viral systems.The Journal of biological chemistry · 2026Review
- REV1‑targeting inhibitor JH‑RE‑06 induces ferroptosis via NCOA4‑mediated ferritinophagy in colorectal cancer cells.Oncology reports · 2025Article
- Sensitization of cancer cells to DNA-damaging agents by expression of the REV1 C-terminal domain: Implications for chemotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Control of Replication Stress Response by Cytosolic Fe-S Cluster Assembly (CIA) Machinery.Cells · 2025Review
- Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Probing hot spots of protein-protein interactions mediated by the safety-belt region of REV7.Structure (London, England : 1993) · 2024Article
- A sophisticated mechanism governs Pol ζ activity in response to replication stress.Nature communications · 2024Article
- Protein Assemblies in Translesion Synthesis.Genes · 2024Review
- Mitochondrial superoxide dismutase Sod2 suppresses nuclear genome instability during oxidative stress.Genetics · 2023Article
- Article
- REV7 in Cancer Biology and Management.Cancers · 2023Review
- The iron-sulfur cluster is essential for DNA binding by human DNA polymerase ε.Scientific reports · 2022Article
- Article
- Post-Translational Modifications of PCNA: Guiding for the Best DNA Damage Tolerance Choice.Journal of fungi (Basel, Switzerland) · 2022Review
- Recent Advances in Understanding the Structures of Translesion Synthesis DNA Polymerases.Genes · 2022Review
- DNA polymerase zeta contributes to heterochromatin replication to prevent genome instability.The EMBO journal · 2021Article
60 more citing papers are in PubMed but not listed here.
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
Abstract
Translesion DNA synthesis is an important branch of the DNA damage tolerance pathway that assures genomic integrity of living organisms. The mechanisms of DNA polymerase (Pol) switches during lesion bypass are not known. Here, we show that the C-terminal domain of the Pol ζ catalytic subunit interacts with accessory subunits of replicative DNA Pol δ. We also show that, unlike other members of the human B-family of DNA polymerases, the highly conserved and similar C-terminal domains of Pol δ and Pol ζ contain a [4Fe-4S] cluster coordinated by four cysteines. Amino acid changes in Pol ζ that prevent the assembly of the [4Fe-4S] cluster abrogate Pol ζ function in UV mutagenesis. On the basis of these data, we propose that Pol switches at replication-blocking lesions occur by the exchange of the Pol δ and Pol ζ catalytic subunits on a preassembled complex of accessory proteins retained on DNA during translesion DNA synthesis.
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.