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- W2015683487 abstract "Significance Oxidative stress is an important contributor to aging-associated diseases including cancer and neurodegeneration, and antioxidant stress responses are critical to limit manifestations of these diseases. We report that the tumor suppressor Homologous to the E6-AP Carboxyl Terminus domain and Ankyrin repeat containing E3 ubiquitin–protein ligase 1 (HACE1) promotes activity of the transcription factor, nuclear factor erythroid 2-related factor 2 (NRF2), a master regulator of the antioxidative stress response. In Huntington disease patients, HACE1 is lost in the brain region most affected by the disease, namely the striatum, and restoring HACE1 functions in striatal cells expressing mutant Huntingtin protein provides protection against oxidative stress. Therefore, the tumor suppressor HACE1 is a new regulator of NRF2 and an emerging player in neurodegeneration." @default.
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- W2015683487 date "2014-02-10" @default.
- W2015683487 modified "2023-10-15" @default.
- W2015683487 title "HACE1 reduces oxidative stress and mutant Huntingtin toxicity by promoting the NRF2 response" @default.
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- W2015683487 doi "https://doi.org/10.1073/pnas.1314421111" @default.
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