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- W2000607329 endingPage "10089" @default.
- W2000607329 startingPage "10074" @default.
- W2000607329 abstract "Extracellular and intracellular oxidants or electrophiles are key contributors to the damages in cellular macromolecules, such as DNA, proteins and lipids. Nrf2 is a master transcription factor that modulates a cellular antioxidant response program and plays an important role in the protection against oxidants and electrophiles. Keap1 is a regulator of Nrf2 by serving as a substrate adaptor for Cullin3-dependent E3 ubiquitin ligase. While Nrf2 activation is a feasible strategy for treatment of age-related diseases, aberrant Nrf2 activation also confers a selective growth advantage of tumor cells during chemotherapy or radiotherapy. In the present review, we provide an overview of the Keap1-Nrf2-ARE system, the domain organization of Nrf2 and Keap1, and the regulatory mechanisms of Nrf2 proteolysis by Keap1. We also discuss how Nrf2 prevents tumor promotion, hampers the sensitivity of selected tumors against chemotherapy or radiotherapy, and reprograms the metabolism to facilitate the tumor proliferation. Finally, we illustrate the current status in the development of Nrf2 chemical activators and inhibitors for the use of potential chemopreventive agents and chemotherapeutic adjuvants, respectively." @default.
- W2000607329 created "2016-06-24" @default.
- W2000607329 creator A5037799804 @default.
- W2000607329 creator A5039921852 @default.
- W2000607329 date "2014-07-10" @default.
- W2000607329 modified "2023-10-17" @default.
- W2000607329 title "Molecular and Chemical Regulation of the Keap1-Nrf2 Signaling Pathway" @default.
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- W2000607329 doi "https://doi.org/10.3390/molecules190710074" @default.
- W2000607329 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6270911" @default.
- W2000607329 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25014534" @default.
- W2000607329 hasPublicationYear "2014" @default.
- W2000607329 type Work @default.
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