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• W2286755989 abstract "Huntington disease (HD) is an incurable brain disorder characterized by the late onset of motor and cognitive symptoms, even though the neurons in the brain begin to suffer dysfunction and degeneration long before symptoms appear. Several molecular and developmental effects of HD have been identified using neural stem cells (NSCs) and differentiated cells, such as neurons and astrocytes. Still, little is known regarding the molecular pathogenesis of HD in pluripotent cells, such as embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). Therefore, we examined putative signaling pathways and processes involved in HD pathogenesis in pluripotent cells. We tested naïve mouse HD YAC128 iPSCs and two types of human HD iPSCs that were generated from HD and juvenile HD patients. Surprisingly, we found that a number of changes affecting cellular processes in HD were also present in undifferentiated pluripotent HD iPSCs, including the deregulation of the MAPK and Wnt signaling pathways and the deregulation of the expression of genes related to oxidative stress, such as Sod1. Interestingly, a common protein interactor of the huntingtin protein and the proteins in the above pathways is p53, and the expression of the p53 gene was deregulated in HD YAC128 iPSCs and human HD iPSCs. In summary, our findings demonstrate that multiple molecular pathways that are characteristically deregulated in HD are already altered in undifferentiated pluripotent cells and that the pathogenesis of HD may begin during the early stages of life." @default.
• W2286755989 created "2016-06-24" @default.
• W2286755989 creator A5007655910 @default.
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• W2286755989 date "2015-01-01" @default.
• W2286755989 modified "2023-09-30" @default.
• W2286755989 title "Huntington disease iPSCs show early molecular changes in intracellular signaling, the expression of oxidative stress proteins and the p53 pathway" @default.
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• W2286755989 doi "https://doi.org/10.1242/dmm.019406" @default.
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