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期刊名称: Trends in Biochemical Sciences
Volume:39    Issue:4        Page:199-218
ISSN:0968-0004

The Nrf2 regulatory network provides an interface between redox and intermediary metabolism期刊论文

作者: Hayes John D Dinkova-Kostova Albena T
DOI:10.1016/j.tibs.2014.02.002

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页码: 199-218
被引频次: 520
出版者: Elsevier Ltd,ELSEVIER SCIENCE LONDON,Elsevier Science Publishers
期刊名称: Trends in Biochemical Sciences
ISSN: 0968-0004
卷期: Volume:39    Issue:4
语言: English
摘要: Nuclear factor-erythroid 2 p45-related factor 2 (Nrf2, also called Nfe212) is a transcription factor that regulates the cellular redox status. Nrf2 is controlled through a complex transcriptional/epigenetic and post-translational network that ensures its activity increases during redox perturbation, inflammation, growth factor stimulation and nutrient/energy fluxes, thereby enabling the factor to orchestrate adaptive responses to diverse forms of stress. Besides mediating stress-stimulated induction of antioxidant and detoxification genes, Nr12 contributes to adaptation by upregulating the repair and degradation of damaged macromolecules, and by modulating intermediary metabolism. In the latter case, Nrf2 inhibits lipogenesis, supports 0-oxidation of fatty acids, facilitates flux through the pentose phosphate pathway, and increases NADPH regeneration and purine biosynthesis; these observations suggest Nrf2 directs metabolic reprogramming during stress.
相关主题: NADPH, Nrf2, thioredoxin, glutathione, Keap1, GSK-3, fatty acid β-oxidation, purine synthesis, β-TrCP, oxidative stress, pentose phosphate pathway, fatty acid 8-oxidation, FACTOR E2-RELATED FACTOR-2, NF-E2-RELATED FACTOR-2 NRF2, BIOCHEMISTRY & MOLECULAR BIOLOGY, beta-TrCP, DIET-INDUCED OBESITY, SELECTIVE AUTOPHAGY, BREAST-CANCER CELLS, Keapl, TRANSCRIPTION FACTOR NRF2, ANTIOXIDANT RESPONSE ELEMENT, FATTY-ACID OXIDATION, GENE-EXPRESSION, NF-KAPPA-B, Metabolic Networks and Pathways, Oxidation-Reduction, Humans, NF-E2-Related Factor 2 - metabolism, Gene Expression Regulation, Lipid Metabolism, NF-E2-Related Factor 2 - genetics, Mitochondria - metabolism,

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