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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Vydáno v:	Biochemical Society transactions Ročník 43; číslo 4; s. 621 - 626
Hlavní autoři:	Wardyn, Joanna D, Ponsford, Amy H, Sanderson, Christopher M
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England 01.08.2015
Témata:	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
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Popis
Shrnutí:	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.
Bibliografie:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1
ISSN:	1470-8752
DOI:	10.1042/BST20150014