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Human PMS1-dependent non-canonical mismatch repair engages with MBD4 to repair methylated CpG deamination.

Nucleic acids research - 10 Aug 2026

Le Ven Anaïs, Vanhuele Sandra, Ganier Olivier, Houy Alexandre, Kahn Amanda, Rodrigues Manuel, Stern Marc-Henri, Guerois Raphael, Silveira André Bortolini

Abstract excerpt

CpG dinucleotides are mutational hotspots due to spontaneous deamination of 5-methylcytosine (5mC), resulting in T:G mismatches that can lead to CpG>TpG transitions. These mutations are a hallmark of aging and cancer and play a central role in the evolution of vertebrate genomes. We have previously uncovered MBD4 as the primary base excision repair (BER) glycosylase responsible for 5mC deamination repair. Here,...

Topics

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5-Methylcytosine
CpG Islands
Deamination
DNA Methylation
DNA Mismatch Repair

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Endodeoxyribonucleases

MutL Protein Homolog 1

Source

Open in PubMed Open full text

Identifiers

PMID: 42578366
DOI: 10.1093/nar/gkag771
PMCID: PMC13458396

Genes

MBD4
PMS1
MLH1
APOBEC1
MSH2
MSH6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

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Human PMS1-dependent non-canonical mismatch repair engages with MBD4 to repair methylated CpG deamination.PMID 42578366Read ↗

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