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Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer
To investigate the role of the presumed DNA mismatch repair (MMR) gene Msh2 in genome stability and tumorigenesis, we have generated cells and mice that are deficient for the gene. Msh2-deficientExpand
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Mouse MutS-like protein Msh5 is required for proper chromosome synapsis in male and female meiosis.
Members of the mammalian mismatch repair protein family of MutS and MutL homologs have been implicated in postreplicative mismatch correction and chromosome interactions during meiotic recombination.Expand
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p107 is a suppressor of retinoblastoma development in pRb-deficient mice.
Hemizygosity for the retinoblastoma gene RB in man strongly predisposes to retinoblastoma. In the mouse, however, Rb hemizygosity leaves the retina normal, whereas in Rb-/- chimeras pRb-deficientExpand
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Tissue-specific tumor suppressor activity of retinoblastoma gene homologs p107 and p130.
The retinoblastoma gene family consists of three genes: RB, p107, and p130. While loss of pRB causes retinoblastoma in humans and pituitary gland tumors in mice, tumorigenesis in other tissues may beExpand
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Targeted gene modification in mismatch-repair-deficient embryonic stem cells by single-stranded DNA oligonucleotides.
Gene targeting through homologous recombination in murine embryonic stem (ES) cells is already strongly suppressed by DNA mismatch-repair (MMR)-dependent anti-recombination when targeting constructExpand
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Msh2 status modulates both apoptosis and mutation frequency in the murine small intestine.
Deficiency in genes involved in DNA mismatch repair increases susceptibility to cancer, particularly of the colorectal epithelium. Using Msh2 null mice, we demonstrate that this genetic defectExpand
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Mouse models for hereditary nonpolyposis colorectal cancer.
Hemizygous germ-line defects in mismatch repair (MMR) genes underlie hereditary nonpolyposis colorectal cancer (HNPCC). Loss of the wild-type allele results in a mutator phenotype, acceleratingExpand
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DNA mismatch repair deficiency stimulates N-ethyl-N-nitrosourea-induced mutagenesis and lymphomagenesis.
The primary role of the mismatch repair (MMR) system is the avoidance of mutations caused by replication and recombination errors. Furthermore, the lethality of methylating agents has been attributedExpand
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Generation of a mouse mutant by oligonucleotide-mediated gene modification in ES cells
Oligonucleotide-mediated gene targeting is emerging as a powerful tool for the introduction of subtle gene modifications in mouse embryonic stem (ES) cells and the generation of mutant mice. However,Expand
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Impact of Ethiopia’s Community Based Health Insurance on household economic welfare
In 2011, the Government of Ethiopia launched a pilot Community-Based Health Insurance (CBHI) scheme. This paper uses three rounds of household survey data, collected before and after the introductionExpand
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