Abstract

Nrf2 and its endogenous inhibitor, Keap1, function as a ubiquitous, evolutionarily conserved intracellular defense mechanism to counteract oxidative stress. Sequestered by cytoplasmic Keap1 and targeted to proteasomal degradation in basal conditions, in case of oxidative stress Nrf2 detaches from Keap1 and translocates to the nucleus, where it heterodimerizes with one of the small Maf proteins. The heterodimers recognize the AREs, that are enhancer sequences present in the regulatory regions of Nrf2 target genes, essential for the recruitment of key factors for transcription. In the present review we briefly introduce the Nrf2-Keap1 system and describe Nrf2 functions, illustrate the Nrf2-NF-κB cross-talk, and highlight the effects of the Nrf2-Keap1 system in the physiology and pathophysiology of striated muscle tissue taking into account its role(s) in oxidative stress and reductive stress.

Keywords

KEAP1Oxidative stressTranscription factorCell biologyBiologyEnhancerOxidative phosphorylationCytoplasmMechanism (biology)EndogenyGeneticsBiochemistryGene

MeSH Terms

Cell NucleusHumansKelch-Like ECH-Associated Protein 1Maf Transcription FactorsNF-E2-Related Factor 2NF-kappa BOxidation-ReductionOxidative StressSignal Transduction

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Publication Info

Year
2018
Type
review
Volume
1865
Issue
5
Pages
721-733
Citations
1803
Access
Closed

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Cite This

Ilaria Bellezza, Ileana Giambanco, Alba Minelli et al. (2018). Nrf2-Keap1 signaling in oxidative and reductive stress. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research , 1865 (5) , 721-733. https://doi.org/10.1016/j.bbamcr.2018.02.010

Identifiers

DOI
10.1016/j.bbamcr.2018.02.010
PMID
29499228

Data Quality

Data completeness: 86%