Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts
Andrew S, Xu X, Baross-Francis A, Narayanan L, Milhausen K, Liskay R, Jirik F, Glazer P. Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts. Carcinogenesis 2000, 21: 1291-1296. PMID: 10874005, DOI: 10.1093/carcin/21.7.1291.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphatasesAnimalsBase Pair MismatchCrosses, GeneticDNA RepairDNA Repair EnzymesDNA-Binding ProteinsFemaleFrameshift MutationGenes, ReporterGenotypeGerm-Line MutationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMismatch Repair Endonuclease PMS2MutagenesisMutS Homolog 2 ProteinPoint MutationProteinsProto-Oncogene ProteinsConceptsPms2-deficient miceMsh2-deficient miceHereditary non-polyposis colorectal cancer patientsCII target geneDNA mismatch repair deficiencyColorectal cancer patientsPMS2 germline mutationsMismatch repair deficiencyReporter transgenic miceMutation frequencyLacI target geneCancer patientsTarget genesMouse modelKnockout miceTumor spectrumTransgenic miceFrameshift mutationGermline mutationsMiceRepair deficiencyPMS2 deficiencySupF target geneMSH2Predominant mutations