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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August 2015
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Review Article|
August 03 2015
Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways
Joanna D. Wardyn;
Joanna D. Wardyn
*University of Liverpool, Cellular and Molecular Physiology, Crown Street, Liverpool L69 3BX, U.K.
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Amy H. Ponsford;
Amy H. Ponsford
*University of Liverpool, Cellular and Molecular Physiology, Crown Street, Liverpool L69 3BX, U.K.
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Christopher M. Sanderson
Christopher M. Sanderson
1
*University of Liverpool, Cellular and Molecular Physiology, Crown Street, Liverpool L69 3BX, U.K.
1To whom correspondence should be addressed (emailcmsand@liverpool.ac.uk).
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Biochem Soc Trans (2015) 43 (4): 621–626.
Article history
Received:
January 14 2015
Citation
Joanna D. Wardyn, Amy H. Ponsford, Christopher M. Sanderson; Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways. Biochem Soc Trans 1 August 2015; 43 (4): 621–626. doi: https://doi.org/10.1042/BST20150014
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