ArticlePLoS genetics2014
The transcription factor TFII-I promotes DNA translesion synthesis and genomic stability.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 44 citations in OpenAlex.
- Cellular transcription factor TFII-I represses adenovirus gene expression.Journal of virology · 2025Article
- Checkpoint activation by Spd1: a competition-based system relying on tandem disordered PCNA binding motifs.Nucleic acids research · 2024Article
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- REV7 in Cancer Biology and Management.Cancers · 2023Review
- A genome-wide screen identifies SCAI as a modulator of the UV-induced replicative stress response.PLoS biology · 2022Article
- Review
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- Autoantibody profiling of alveolar rhabdomyosarcoma patients unveils tumor-associated antigens with diagnostic and prognostic significance.Oncoimmunology · 2021Article
- Regulation of RNA Polymerase II Transcription Initiation and Elongation by Transcription Factor TFII-I.Frontiers in molecular biosciences · 2021Review
- Mutant GTF2I induces cell transformation and metabolic alterations in thymic epithelial cells.Cell death and differentiation · 2020Article
- Peptides containing the PCNA interacting motif APIM bind to the β-clamp and inhibit bacterial growth and mutagenesis.Nucleic acids research · 2020Article
- Helicase-Like Transcription Factor HLTF and E3 Ubiquitin Ligase SHPRH Confer DNA Damage Tolerance through Direct Interactions with Proliferating Cell Nuclear Antigen (PCNA).International journal of molecular sciences · 2020Article
- Structure and function relationships in mammalian DNA polymerases.Cellular and molecular life sciences : CMLS · 2020Review
- Targeting the non-canonical roles of PCNA modifies and increases the response to targeted anti-cancer therapy.Oncotarget · 2019Article
- "Two hits - one stone"; increased efficacy of cisplatin-based therapies by targeting PCNA's role in both DNA repair and cellular signaling.Oncotarget · 2018Article
- 53BP1 cooperation with the REV7-shieldin complex underpins DNA structure-specific NHEJ.Nature · 2018Article
- The role of PCNA as a scaffold protein in cellular signaling is functionally conserved between yeast and humans.FEBS open bio · 2018Article
- FAM35A associates with REV7 and modulates DNA damage responses of normal and BRCA1-defective cells.The EMBO journal · 2018Article
- Structure of proliferating cell nuclear antigen (PCNA) bound to an APIM peptide reveals the universality of PCNA interaction.Acta crystallographica. Section F, Structural biology communications · 2018Article
- APIM-peptide targeting PCNA improves the efficacy of docetaxel treatment in the TRAMP mouse model of prostate cancer.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Translesion synthesis (TLS) enables DNA replication through damaged bases, increases cellular DNA damage tolerance, and maintains genomic stability. The sliding clamp PCNA and the adaptor polymerase Rev1 coordinate polymerase switching during TLS. The polymerases Pol η, ι, and κ insert nucleotides opposite damaged bases. Pol ζ, consisting of the catalytic subunit Rev3 and the regulatory subunit Rev7, then extends DNA synthesis past the lesion. Here, we show that Rev7 binds to the transcription factor TFII-I in human cells. TFII-I is required for TLS and DNA damage tolerance. The TLS function of TFII-I appears to be independent of its role in transcription, but requires homodimerization and binding to PCNA. We propose that TFII-I bridges PCNA and Pol ζ to promote TLS. Our findings extend the general principle of component sharing among divergent nuclear processes and implicate TLS deficiency as a possible contributing factor in Williams-Beuren syndrome.
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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.