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

Wardyn JD, Ponsford AH, Sanderson CM - Biochem. Soc. Trans. (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: University of Liverpool, Cellular and Molecular Physiology, Crown Street, Liverpool L69 3BX, U.K.

No MeSH data available.


Related in: MedlinePlus

Well-characterized points of molecular cross-talk between NF-κB and Nrf2 response pathways
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Figure 1: Well-characterized points of molecular cross-talk between NF-κB and Nrf2 response pathways

Mentions: HO-1 is an Nrf2 target gene, which is at the core of Nrf2-mediated NF-κB inhibition. This enzyme is involved in haeme metabolism by catalysing the cleavage of the porphyrin ring of haeme into Fe2+, carbon monoxide and biliverdin, which is consequently converted into bilirubin. Increases in HO-1 activity in endothelial cells leads to inhibition of NF-κB-mediated transcription of adhesion molecules such as E-Selectin and vascular cell adhesion molecule 1 (VCAM-1), through the action of bilirubin and possibly by the decrease in free intracellular iron ions [30]. A summary of known points of molecular cross-talk between Nrf2 and NF-κB is presented in Figure 1.


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

Wardyn JD, Ponsford AH, Sanderson CM - Biochem. Soc. Trans. (2015)

Well-characterized points of molecular cross-talk between NF-κB and Nrf2 response pathways
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4613495&req=5

Figure 1: Well-characterized points of molecular cross-talk between NF-κB and Nrf2 response pathways
Mentions: HO-1 is an Nrf2 target gene, which is at the core of Nrf2-mediated NF-κB inhibition. This enzyme is involved in haeme metabolism by catalysing the cleavage of the porphyrin ring of haeme into Fe2+, carbon monoxide and biliverdin, which is consequently converted into bilirubin. Increases in HO-1 activity in endothelial cells leads to inhibition of NF-κB-mediated transcription of adhesion molecules such as E-Selectin and vascular cell adhesion molecule 1 (VCAM-1), through the action of bilirubin and possibly by the decrease in free intracellular iron ions [30]. A summary of known points of molecular cross-talk between Nrf2 and NF-κB is presented in Figure 1.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: University of Liverpool, Cellular and Molecular Physiology, Crown Street, Liverpool L69 3BX, U.K.

No MeSH data available.


Related in: MedlinePlus