ArticleCell2025
DNA mutagenesis driven by transcription factor competition with mismatch repair.
Article in Cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Who cites it
6 citing papers in PubMed.
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Nature communications · 2026Article
- DNA Mechanical Strain Steers Transcription Factor Recognition.Research square · 2026Article
- Article
- Relationship between MLH1, MSH2, MSH6, and PMS2 protein expression status and clinicopathological characteristics in colorectal cancer tissues.Frontiers in medicine · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Research square · 2025Article
- From Transcription Factors Dysregulation to Malignancy: In Silico Reconstruction of Cancer's Foundational Drivers-The Eternity Triangle.International journal of molecular sciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Despite the remarkable fidelity of eukaryotic DNA replication, nucleotide misincorporation errors occur in every replication cycle, generating mutations that drive genetic diseases and genome evolution. Here, we show that transcription factor (TF) proteins, key players in gene regulation, can increase mutagenesis from replication errors by directly competing with the recognition of DNA mismatches by MutSα, the primary initiator of eukaryotic mismatch repair (MMR). We demonstrate this TF-induced mutagenesis mechanism using a yeast genetic assay that quantifies the accumulation of mutations in TF binding sites. Analyses of human cancer mutations recapitulate the trends observed in yeast, with mutations arising from MYC-bound mismatches being enriched in MMR-proficient cells. These findings implicate TF-MMR competition as a critical determinant of somatic hypermutation at TF binding sites in cancer. Furthermore, our results provide a molecular mechanism for the higher-than-expected rate of rare genetic variants at TF binding sites, with important implications for regulatory DNA evolution.
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Registered trials
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