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RELA — SYK
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Takada et al., J Biol Chem 2003
:
First, H2O2 activated Syk in KBM-5 cells ; second, H2O2 failed to activate NF-kappaB in cells that do not express Syk protein ; third, overexpression of
Syk increased H2O2 induced
NF-kappaB activation ; and fourth, reduction of Syk transcription using small interfering RNA inhibited H2O2 induced NF-kappaB activation
Takada et al., J Immunol 2004
:
Jurkat cells that did not express Syk ( JCaM1, JCaM1/lck ) showed lack of TNF induced
Syk , JNK, p38 MAPK, and p44/p42 MAPK activation, as well as TNF induced IkappaBalpha phosphorylation, IkappaBalpha degradation, and
NF-kappaB activation ... TNF induced
NF-kappaB activation was
enhanced by overexpression of
Syk by Syk-cDNA and suppressed when Syk expression was down-regulated by expression of Syk-small interfering RNA ( siRNA-Syk ) ... The apoptotic effects of TNF were reduced by
up-regulation of
NF-kappaB by
Syk-cDNA , and enhanced by down-regulation of NF-kappaB by siRNA-Syk ... Overall, our results demonstrate that
Syk activation
plays an essential role in TNF induced activation of JNK, p38 MAPK, p44/p42 MAPK,
NF-kappaB , and apoptosis
Ulanova et al., Biochem Biophys Res Commun 2006
:
Inhibition of
Syk down-regulated TNF induced p38 and p44/42 MAPK phosphorylation and nuclear translocation of p65
NF-kappaB
Gallagher et al., J Neurosci 2007
:
CNTF induced SYK phosphorylation is rapidly followed by increased tyrosine phosphorylation of IkappaB-alpha, and blocking
SYK activation or tyrosine phosphorylation of IkappaB-alpha
prevents CNTF induced
NF-kappaB activation and CNTF promoted neurite growth
Oh et al., J Biol Chem 2007
:
Inhibition of the activity of
Syk prior to, concomitant with or shortly following receptor engagement led to the rapid inhibition of receptor mediated tyrosine phosphorylation and
blocked the activation of extracellular signal regulated kinase,
NF-kappaB , and NFAT ... The receptor mediated activation of
NF-kappaB required active
Syk for a relatively short period of time, whereas the activation of NFAT required active kinase for a prolonged ( > 1 h ) period
Bijli et al., J Biol Chem 2008
:
Consistent with this, thrombin induced
NF-kappaB activity and ICAM-1 expression were
prevented by the expression of a kinase-defective mutant or RNA interference knockdown of
Syk ... Analysis of the NF-kappaB pathway showed that
Syk contributes to thrombin induced
NF-kappaB activation by controlling its transactivation potential and that this response is associated with tyrosine phosphorylation of RelA/p65
Bi et al., J Biol Chem 2010
:
The scaffold protein CARD9 plays an essential role in anti-fungus immunity and is implicated in mediating
Dectin-1/Syk induced
NF-kappaB activation in response to Candida albicans infection ... Finally, we find that although both CARD9 and
Syk are
required for Hyphae induced
NF-kappaB activation, they regulate different signaling events in which CARD9 mediates IkappaBalpha kinase ubiquitination, whereas Syk regulates IkappaBalpha kinase phosphorylation
Ho et al., Nat Immunol 2012
(Inflammation) :
Here we found lipopolysaccharide stimulation of kinase
Syk mediated tyrosine phosphorylation of RIP140 and interaction of the NF-?B subunit
RelA with RIP140