beta-catenin promotes NLRP3 inflammasome activation. When expression of beta-catenin suppressed by siRNA or pharmacological inhibitor the NLRP3 inflammasome activation was impaired. Accordingly beta-catenin inhibitor attenuated LPS-induced systemic inflammation in vivo. beta-catenin interacted with NLRP3 and promoted the association between NLRP3 and ASC.
oligomerization of ASC creates a multitude of potential caspase-1 activation sites thus serving as a signal amplification mechanism for inflammasome-mediated cytokine production
IKKalpha controls the inflammasome at the level of the adaptor molecule ASC which interacts with IKKalpha in the nucleus of resting macrophages in an IKKalpha kinase-dependent manner.
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