ArticleGenes to cells : devoted to molecular & cellular mechanisms2009
Identification of a novel REV1-interacting motif necessary for DNA polymerase kappa function.
Article in Genes to cells : devoted to molecular & cellular mechanisms, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 99 citations in OpenAlex.
- Overlapping RAD18-and DNA-binding interfaces in DNA polymerase η contribute to UV-induced DNA damage tolerance.The Journal of biological chemistry · 2026Article
- Human REV1 interacts with DHX36 to promote replication and tolerance of G-quadruplex DNA.Nucleic acids research · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs.Nucleic acids research · 2025Article
- Catalytic and noncatalytic functions of DNA polymerase κ in translesion DNA synthesis.Nature structural & molecular biology · 2025Article
- Bypass of Methoxyamine-Adducted Abasic Sites by Eukaryotic Translesion DNA Polymerases.International journal of molecular sciences · 2025Article
- Protein Assemblies in Translesion Synthesis.Genes · 2024Review
- E3 ubiquitin ligase RNF2 protects polymerase ι from destabilization.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Rev1 overexpression accelerates N-methyl-N-nitrosourea (MNU)-induced thymic lymphoma by increasing mutagenesis.Cancer science · 2024Article
- Lead compound profiling for small molecule inhibitors of the REV1-CT/RIR Translesion synthesis Protein-Protein interaction.Bioorganic & medicinal chemistry · 2024Article
- A Novel Interaction Between RAD23A/B and Y-family DNA Polymerases.Journal of molecular biology · 2023Article
- Post-Translational Modifications of PCNA: Guiding for the Best DNA Damage Tolerance Choice.Journal of fungi (Basel, Switzerland) · 2022Review
- Genetic and physical interactions between Polη and Rev1 in response to UV-induced DNA damage in mammalian cells.Scientific reports · 2021Article
- Protein-Protein Interactions in Translesion Synthesis.Molecules (Basel, Switzerland) · 2021Review
- Targeting protein-protein interactions in the DNA damage response pathways for cancer chemotherapy.RSC chemical biology · 2021Review
- Structure-Based Drug Design of Phenazopyridine Derivatives as Inhibitors of Rev1 Interactions in Translesion Synthesis.ChemMedChem · 2021Article
- Mechanisms for Maintaining Eukaryotic Replisome Progression in the Presence of DNA Damage.Frontiers in molecular biosciences · 2021Review
- Translesion synthesis inhibitors as a new class of cancer chemotherapeutics.Expert opinion on investigational drugs · 2021Review
- A stapled POL κ peptide targets REV1 to inhibit mutagenic translesion synthesis.Environmental and molecular mutagenesis · 2020Article
- The in vivo role of Rev1 in mutagenesis and carcinogenesis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2020Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
When a replicative DNA polymerase (Pol) is stalled by damaged DNA, a "polymerase switch" recruits specialized translesion synthesis (TLS) DNA polymerase(s) to sites of damage. Mammalian cells have several TLS DNA polymerases, including the four Y-family enzymes (Poleta, Poliota, Polkappa and REV1) that share multiple primary sequence motifs, but show preferential bypass of different DNA lesions. REV1 interacts with Poleta, Poliota, and Polkappa and therefore appears to play a central role during TLS in vivo. Here we have investigated the molecular basis for interactions between REV1 and Polkappa. We have identified novel REV1-interacting regions (RIRs) present in Polkappa, Poliota and Poleta. Within the RIRs, the presence of two consecutive phenylalanines (FF) is essential for REV1-binding. The consensus sequence for REV1-binding is denoted by x-x-x-F-F-y-y-y-y (x, no specific residue and y, no specific residue but not proline). Our results identify structural requirements that are necessary for FF-flanking residues to confer interactions with REV1. A Polkappa mutant lacking REV1-binding activity did not complement the genotoxin-sensitivity of Polk-null mouse embryonic fibroblast cells, thereby demonstrating that the REV1-interaction is essential for Polkappa function in vivo.
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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.