ArticleOncogene2002
Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Adult glioblastoma with Lynch syndrome-associated mismatch repair deficiency forms a distinct high-risk molecular subgroup.Free neuropathology · 2024Article
- Deficiency of replication-independent DNA mismatch repair drives a 5-methylcytosine deamination mutational signature in cancer.Science advances · 2021Article
- Serrated polyposis associated with a family history of colorectal cancer and/or polyps: The preferential location of polyps in the colon and rectum defines two molecular entities.International journal of molecular medicine · 2016Article
- Deficiency of the DNA repair protein nibrin increases the basal but not the radiation induced mutation frequency in vivo.Mutation research · 2014Article
- Integrated exome and transcriptome sequencing reveals ZAK isoform usage in gastric cancer.Nature communications · 2014Article
- TagRecon: high-throughput mutation identification through sequence tagging.Journal of proteome research · 2010Article
- Mutagenicity and potential carcinogenicity of thiopurine treatment in patients with inflammatory bowel disease.Cancer research · 2009Article
- Role of the mismatch repair gene, Msh6, in suppressing genome instability and radiation-induced mutations.Mutation research · 2008Article
- Evidence for mutation showers.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6.Carcinogenesis · 2006Article
- The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation.Genetics · 2006Article
- A hypermutation phenotype and somatic MSH6 mutations in recurrent human malignant gliomas after alkylator chemotherapy.Cancer research · 2006Article
- Gene expression profiling of naïve sheep genetically resistant and susceptible to gastrointestinal nematodes.BMC genomics · 2006Article
- Mutation rates, spectra and hotspots in mismatch repair-deficient Caenorhabditis elegans.Genetics · 2005Article
- Article
- Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The DNA mismatch repair (MMR) system is primarily responsible for purging newly synthesized DNA of errors incurred during semi-conservative replication. Lesion recognition is initially carried out by one of two heterodimeric protein complexes, MutS(alpha) or MutS(beta). While the former, comprised of MSH2 and MSH6, recognizes mispairs as well as short (1-2 nucleotide) insertions/deletions (IDLs), the latter, made up of MSH2 and MSH3, is primarily responsible for recognizing 2-6 nucleotide IDLs. As most of the functional information on these heterodimers is derived from in vitro studies, it was of interest to study the in vivo consequences of a lack of MutS(alpha). To this end, Big Blue( trade mark ) mice, that carry a lacI(+) transgenic lambda shuttle-phage mutational reporter, were crossed with Msh6(-/-) mice to evaluate the specific contribution of MutS(alpha) to genome integrity. Consistent with the importance of MutS(alpha) in lesion surveillance, small intestine epithelial cell DNA derived from lacI(+) Msh6(-/-) mice exhibited striking increases (average of 41-fold) in spontaneous mutant frequencies. Furthermore, the lacI gene mutation spectrum was dominated by G:C to A:T transitions, highlighting the critical importance of the MutS(alpha) complex in suppressing this frequently observed type of spontaneous mutation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.