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

Role of the Msh2 gene in genome maintenance and development in mouse fetuses.

Mutation research - 1 Jun 2012

He Dongwei, Chen Yali, Li Huiying, Furuya Maiko, Ikehata Hironobu, Uehara Yoshihiko, Komura Jun-ichiro, Mak Tak W, Ono Tetsuya

Abstract excerpt

In an attempt to evaluate the roles of the mismatch repair gene Msh2 in genome maintenance and in development during the fetal stage, spontaneous mutations and several developmental indices were studied in Msh2-deficient lacZ-transgenic mouse fetuses. Mutation levels in fetuses were elevated at 9.5 dpc (days post coitum) when compared to wild-type mice, and the level of mutations continued to increase until the...

Read the complete abstract on PubMed

Topics

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

Share to DNA Repair
Share to DNA Replication

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fetal Development

Share to Mice, Transgenic

Share to Mutation Rate

Share to MutS Homolog 2 Protein

Source

Identifiers

PMID: 22465156
DOI: 10.1016/j.mrfmmm.2012.03.004

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Role of the Msh2 gene in genome maintenance and development in mouse fetuses.PMID 22465156Read ↗

High Mutation Levels are Compatible with Normal Embryonic Development in Mlh1-Deficient Mice.Semantic proximity Read ↗

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

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

Maternal effect for DNA mismatch repair in the mouse.Semantic proximity Read ↗

Role of MUTYH and MSH2 in the control of oxidative DNA damage, genetic instability, and tumorigenesis.Semantic proximity Read ↗

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

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

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

Mice defective in the DNA mismatch gene PMS2 are hypersensitive to MNU induced thymic lymphoma and are partially protected by transgenic expression of human MGMT.Semantic proximity Read ↗

Mouse models for human DNA mismatch-repair gene defects.Semantic proximity Read ↗

Tissue-specific mismatch repair protein expression: MSH3 is higher than MSH6 in multiple mouse tissuesSemantic proximity Read ↗

Thymic lymphomas arising in Msh2 deficient mice display a large increase in mutation frequency and an altered mutational spectrum.Semantic proximity Read ↗

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