NF-kappaB/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK.

By Guang-Hui Liu, J. Qu, Xun Shen. Biochimica et Biophysica Acta, 2008

691 citations recorded by the source corpus.

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When NRF2 Talks, Who's Listening? (2010, positive): “The loss of CBP from the MafK-NRF2 heterodimer may then cause destabilization and allow HDAC3 to bind and deacetylate MafK.”
Oxidative Stress in Cancer (2020, background): “…(Paul et al., 2018) and overexpression of the NF-κB p65/RelA subunit antagonizes NRF2 by depriving it of CBP and recruiting histone deacetylase 3 (Liu et al., 2008) and that, when oxidative stress is sufficient to cause DNA damage, the ensuing activation of TP53 results in antagonism of NRF2,…”
Activation of Nrf2-antioxidant signaling attenuates NF-κB-inflammatory response and elicits apoptosis (2008, background): “[21] Liu GH, Qu J, Shen X. NF-kappaB/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK.”
NF-κB in Oxidative Stress (2017, background): “On the other hand, NF-κB inhibits Nrf2 by competing for the transcriptional co-activator CBP (CREB-binding protein)–p300 complex [30].”