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

A naturally occurring hPMS2 mutation can confer a dominant negative mutator phenotype.

Molecular and cellular biology - 1 Mar 1998

Nicolaides N C, Littman S J, Modrich P, Kinzler K W, Vogelstein B

Abstract excerpt

Defects in mismatch repair (MMR) genes result in a mutator phenotype by inducing microsatellite instability (MI), a characteristic of hereditary nonpolyposis colorectal cancers (HNPCC) and a subset of sporadic colon tumors. Present models describing the mechanism by which germ line mutations in MMR genes predispose kindreds to HNPCC suggest a "two-hit" inactivation of both alleles of a particular MMR gene. Here...

Read the complete abstract on PubMed

Topics

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

Share to Bacterial Proteins
Share to Cell Line
Share to Cricetinae

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA-Binding Proteins

Share to DNA Repair

Share to Escherichia coli Proteins

Share to HeLa Cells

Share to Mutation

Source

Open in PubMed Open full text

Identifiers

PMID: 9488480
DOI: 10.1128/MCB.18.3.1635
PMCID: PMC108878

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

A naturally occurring hPMS2 mutation can confer a dominant negative mutator phenotype.PMID 9488480Read ↗

Functional consequences of DNA mismatch repair missense mutations in murine models and their impact on cancer predisposition.Semantic proximity Read ↗

Mutations predisposing to hereditary nonpolyposis colorectal cancer.Semantic proximity Read ↗

Molecular basis of HNPCC: mutations of MMR genes.Semantic proximity Read ↗

Molecular models for the tissue specificity of DNA mismatch repair-deficient carcinogenesis.Semantic proximity Read ↗

Overexpression of the DNA mismatch repair factor, PMS2, confers hypermutability and DNA damage tolerance.Semantic proximity Read ↗

Frequency and types of spontaneous Hprt lymphocyte mutations in Pms2-deficient mice.Semantic proximity Read ↗

The selection for mismatch repair defects in hereditary nonpolyposis colorectal cancer: revising the mutator hypothesis.Semantic proximity Read ↗

The role of hPMS1 and hPMS2 in predisposing to colorectal cancer.Semantic proximity Read ↗

Lack of DNA mismatch repair protein MSH6 in the rat results in hereditary non-polyposis colorectal cancer-like tumorigenesis.Semantic proximity Read ↗

A novel mouse model of PMS2 founder mutation that causes mismatch repair defect due to aberrant splicing.Semantic proximity Read ↗

Constitutive deficiency in DNA mismatch repair: is it time for Lynch III?Semantic proximity Read ↗

Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancer.Semantic proximity Read ↗

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