2.7.11.10	ATP + a protein	CHUK associates with the NF-kappaB inhibitory protein, IkappaB-alpha, in mammalian cells. CHUK specifically phosphorylates IkappaB-alpha on both Ser32 and Ser36, modifications that are required for targeted degradation of IkappaB-alpha via the ubiquitin-proteasome pathway	
2.7.11.10	ATP + a protein	the I kappa B/NF-kappa B system is a key determinant of mucosal inflammation and protection	
2.7.11.10	ATP + a protein	the expression of pkn1 is developmentally regulated to start immediately before spore formation. The enzyme plays an important role in the onset of proper differentiation	
2.7.11.10	ATP + a protein	phosphorylation of IkappaBs marks them out for destruction, thereby relieving their inhibitory effect on NF-kappaB	
2.7.11.10	ATP + a protein	phosphorylates IkappaB inhibitory proteins, causing their degradation and activation of transcription factor NF-kappaB, a master activator of inflammatory responses	
2.7.11.10	ATP + Bcl	phosphorylation at the C-terminus of Bcl by IKKbeta disrupts Bcl10/Malt1 association and Bcl10-mediated signaling	
2.7.11.10	ATP + Bcl10	negative regulatory activity of the IKK complex in Bcl10 degradation, which is part of the regulatory mechanisms that precisely control the response to antigens, overview	
2.7.11.10	ATP + IkappaB protein	the enzyme targets the inhibitory IkappaB protein tightly bound to the transcription factor NF-kappaB for proteasomal degradation and allows the freed NF-kappaB to enter the nucleus where it can be transactivate its target gene, IKKalpha is involved in inflammation in macrophages	
2.7.11.10	ATP + IkappaBalpha	-	
2.7.11.10	ATP + IkappaBalpha	a step in NF-kappaB activation, the IKK complex, composed of IKKalpha, IKKbeta, and NEMO/IKKgamma, is the convergence point for many diverse NFkappaB-activating stimuli including TNFalpha, LPS, and IL-1, overview, IKKbeta is the primary positive regulator of NFkappaB activity in inflammatory processes, is the molecular link between inflammation and cancer