Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways

In most tissues, cells are exposed to frequent changes in levels of oxidative stress and inflammation. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and nuclear factor-κB (NF-κB) are the two key transcription factors that regulate cellular responses to oxidative stress and inflammation respecti...

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Bibliographic Details
Published in:Biochemical Society transactions Vol. 43; no. 4; pp. 621 - 626
Main Authors: Wardyn, Joanna D, Ponsford, Amy H, Sanderson, Christopher M
Format: Journal Article
Language:English
Published: England 01.08.2015
Subjects:
Animals
Cytokines - metabolism
Gene Expression Regulation
Humans
Nervous System Diseases - drug therapy
Nervous System Diseases - genetics
Nervous System Diseases - metabolism
NF-E2-Related Factor 2 - genetics
NF-E2-Related Factor 2 - metabolism
NF-kappa B - metabolism
Oxidative Stress
Signal Transduction
Kelch-like ECH-associated protein 1 (Keap1)
neurodegeneration
inhibitor of kappa light polypeptide gene enhancer in B-cells kinase beta (IKKβ)
haeme oxygenase-1 (HO-1)
nuclear factor (erythroid-derived 2)-like 2 (Nrf2)
nuclear factor-κB (NF-κB)
ISSN:1470-8752
Online Access:Get more information
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Summary:In most tissues, cells are exposed to frequent changes in levels of oxidative stress and inflammation. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and nuclear factor-κB (NF-κB) are the two key transcription factors that regulate cellular responses to oxidative stress and inflammation respectively. Pharmacological and genetic studies suggest that there is functional cross-talk between these two important pathways. The absence of Nrf2 can exacerbate NF-κB activity leading to increased cytokine production, whereas NF-κB can modulate Nrf2 transcription and activity, having both positive and negative effects on the target gene expression. This review focuses on the potentially complex molecular mechanisms that link the Nrf2 and NF-κB pathways and the importance of designing more effective therapeutic strategies to prevent or treat a broad range of neurological disorders.
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ISSN:1470-8752
DOI:10.1042/BST20150014