Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer.

doi:10.1016/0092-8674(95)90319-4

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Article

Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer.

Cell - 28 Jul 1995

de Wind N, Dekker M, Berns A, Radman M, te Riele H

Abstract excerpt

To investigate the role of the presumed DNA mismatch repair (MMR) gene Msh2 in genome stability and tumorigenesis, we have generated cells and mice that are deficient for the gene. Msh2-deficient cells have lost mismatch binding and have acquired microsatellite instability, a mutator phenotype, and tolerance to methylating agents. Moreover, in these cells, homologous recombination has lost dependence on complete...

Topics

Animals
Base Composition
Base Sequence
Chimera
DNA
DNA Repair
DNA-Binding Proteins
Fungal Proteins
Genetic Predisposition to Disease
Lymphoma
Methylation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Methylnitronitrosoguanidine

Mice

Mice, Mutant Strains

Molecular Sequence Data

MutS Homolog 2 Protein

Mutagenesis

Oligodeoxyribonucleotides

Source

Open in PubMed

Identifiers

PMID: 7628020
DOI: 10.1016/0092-8674(95)90319-4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7628020-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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