Selective inhibition of NF-κB activation by a peptide that blocks the interaction of NEMO with the IκB kinase complex

By M. May, F. D’Acquisto, L. Madge, J. Glöckner, J. Pober, S. Ghosh. 2000

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T Cell-Intrinsic Requirement for NF-κB Induction in Postdifferentiation IFN-γ Production and Clonal Expansion in a Th1 Response1 (2003, methodology): “This decrease in Bcl-3 levels was also observed in experiments performed using a specific IKK inhibitor peptide (30) (200 M) vs DMSO vehicle, data not shown).”
Requirement of Hsp90 activity for IκB kinase (IKK) biosynthesis and for constitutive and inducible IKK and NF-κB activation (2004, background): “IKKg is essential for activation of the kinase complex by proinflammatory stimuli and sequesters IKKa and IKKb homo or heterodimers through an N-terminal domain, which binds to a short C-terminal segment present in each kinase (May et al., 2000).”
Roles of NF-κB in Cancer and Inflammatory Diseases and Their Therapeutic Approaches (2016, background): “The degradation of IκBα is mediated by phosphorylation through the IκB kinase (IKK), a trimeric complex composed of two catalytic subunits, IKKα and IKKβ, and a regulatory subunit, IKKγ (also termed NF-κB essential modulator or NEMO) [21].”