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CHUK — SYT1

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Yang et al., J Immunol 2003 : Using mouse embryonic fibroblasts lacking either IKK alpha or IKK beta, we found that IKK beta played an essential role in LPS induced p65 phosphorylation on serine 536, while IKK alpha was partially required for the p65 phosphorylation
Grundström et al., J Biol Chem 2004 : Impaired translocation of the p65 subunit in tolerant T cells was a result from reduced activation of IkappaB kinase and poor phosphorylation and degradation of cytosolic IkappaBs
Kim et al., Cell Signal 2007 (Cell Transformation, Viral) : Pharmacological inhibition of IKKalpha/beta activity reduced both Zn2+ induced p65/RelA phosphorylation at Ser 536 and NF-kappaB dependent transcriptional activity, suggesting that IKKalpha/beta is necessary for these Zn2+ induced effects
Gloire et al., J Biol Chem 2007 : We conclude that nuclear IKKalpha is required for p65 DNA binding in a gene-specific manner
Bednarski et al., Mol Cancer Ther 2008 : However, a decrease in either IKKalpha or IKKbeta resulted in decreased phosphorylation of p65 in response to doxorubicin
Wu et al., Free Radic Biol Med 2009 (Inflammation...) : Collectively, the results of this study and those of previous reports indicate that the conversion of cardiomyocytes to a proinflammatory phenotype in sepsis involves two distinct pathways : NADPH oxidase mediated phosphorylation of IKK and p38 MAP kinase mediated phosphorylation of p65