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• W2000543353 abstract "Msh2 is a key mammalian DNA mismatch repair (MMR) gene and mutations or deficiencies in mammalian Msh2 gene result in microsatellite instability (MSI+) and the development of cancer. Here, we report that primary mouse embryonic fibroblasts (MEFs) deficient in the murine MMR gene Msh2 (Msh2−/−) showed a significant increase in chromosome aneuploidy, centrosome amplification, and defective mitotic spindle organization and unequal chromosome segregation. Although Msh2−/− mouse tissues or primary MEFs had no apparent change in telomerase activity, telomere length, or recombination at telomeres, Msh2−/− MEFs showed an increase in chromosome end-to-end fusions or chromosome ends without detectable telomeric DNA. These data suggest that MSH2 helps to maintain genomic stability through the regulation of the centrosome and normal telomere capping in vivo and that defects in MMR can contribute to oncogenesis through multiple pathways." @default.
• W2000543353 created "2016-06-24" @default.
• W2000543353 creator A5003585920 @default.
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• W2000543353 creator A5057778361 @default.
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• W2000543353 date "2005-12-05" @default.
• W2000543353 modified "2023-10-17" @default.
• W2000543353 title "Msh2 deficiency leads to chromosomal abnormalities, centrosome amplification, and telomere capping defect" @default.
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• W2000543353 doi "https://doi.org/10.1038/sj.onc.1209277" @default.
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