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- W2024677034 abstract "Huntington's disease (HD) is a signature polyglutamine disorder. An enduring theory of HD pathogenesis has involved dysregulation of transcription. Indeed, transcriptional regulatory proteins can be modulated to overcome cardinal features of HD-modeled mice, and efforts to move these into human studies are ongoing. Here, we discuss a unifying hypothesis emerging from these studies, which is that HD represents the pathological disruption of evolutionarily conserved adaptive gene programs to counteract oxidative stress, mitochondrial dysfunction and accumulation of misfolded proteins. Transcriptional dyshomeostasis of adaptive genes is further exacerbated by repression of genes involved in normal synaptic activity or growth factor signaling." @default.
- W2024677034 created "2016-06-24" @default.
- W2024677034 creator A5016406756 @default.
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- W2024677034 date "2014-07-01" @default.
- W2024677034 modified "2023-09-27" @default.
- W2024677034 title "Transcriptional dysregulation in Huntington's disease: a failure of adaptive transcriptional homeostasis" @default.
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- W2024677034 doi "https://doi.org/10.1016/j.drudis.2014.03.016" @default.
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