Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Msh-2 suppresses in vivo mutation in a gene dose and lesion dependent manner.

Oncogene - 14 Jun 2001

Sansom O J, Toft N J, Winton D J, Clarke A R

Abstract excerpt

Mice deficient for the mismatch repair (MMR) gene Msh2 show accelerated tumourigenesis and a reduced apoptotic response to DNA damage of methylation type. Here we examine the effect of mutation for Msh2 on in vivo mutation frequencies in the intestine as determined by loss of function at the Dolichos biflorus (Dlb-1) locus. Spontaneous mutation frequencies were scored in cohorts of ageing mice either wild type or...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Base Pair Mismatch
Share to Cisplatin
Share to DNA Repair

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Dosage

Share to Methylnitronitrosoguanidine

Share to Mutagenesis

Share to MutS Homolog 2 Protein

Share to Proto-Oncogene Proteins

Source

Identifiers

PMID: 11429706
DOI: 10.1038/sj.onc.1204449

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Msh-2 suppresses in vivo mutation in a gene dose and lesion dependent manner.PMID 11429706Read ↗

Apoptosis and mutation in the murine small intestine: loss of Mlh1- and Pms2-dependent apoptosis leads to increased mutation in vivo.Semantic proximity Read ↗

Base transitions dominate the mutational spectrum of a transgenic reporter gene in MSH2 deficient mice.Semantic proximity Read ↗

Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6.Semantic proximity Read ↗

Msh2 deficiency increases the mutation frequency in all parts of the mouse colon.Semantic proximity Read ↗

An Msh2 Point Mutation Uncouples DNA Mismatch Repair and ApoptosisSemantic proximity Read ↗

Oxidative Stress Accelerates Repeat Instability and Base Substitutions, Promoting Gastrointestinal Driver Mutations under MSH2 DeficiencySemantic proximity Read ↗

Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2.Semantic proximity Read ↗

MSH2 deficient mice are viable and susceptible to lymphoid tumours.Semantic proximity Read ↗

Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium.Semantic proximity Read ↗

Tumour susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair.Semantic proximity Read ↗

Different mutator phenotypes in Mlh1- versus Pms2-deficient mice.Semantic proximity Read ↗

Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.