◀ Back to CHUK
CHUK — SYT1
Text-mined interactions from Literome
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