◀ Back to JUN
JUN — SYK
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Arndt et al., J Biol Chem 2004
:
Lipopolysaccharide induced
c-Jun NH2-terminal kinase activation in human neutrophils :
role of phosphatidylinositol 3-Kinase and
Syk mediated pathways
Cha et al., J Pharmacol Exp Ther 2006
:
A novel
spleen tyrosine kinase inhibitor
blocks c-Jun N-terminal kinase mediated gene expression in synoviocytes ... Western blot analysis demonstrated that
Syk inhibition by R406 markedly
suppressed TNFalpha induced
c-Jun N-terminal kinase (JNK) phosphorylation in FLS, with a modest decrease in extracellular signal regulated kinase phosphorylation
Kim et al., FEBS Lett 2012
(Atherosclerosis) :
ROS mediated c-Jun NH ( 2 ) -terminal kinase ( JNK ) is also required for AP-1 activation, but
Syk and PI3K
regulated AP-1 activation independently of JNK
Ghosh et al., J Biol Chem 2012
(Calcium Signaling...) :
In the present study, we found that
Syk is
regulated by the transcription factor
c-Jun in cooperation with Ets2 ... Disruption of
c-Jun and Ets2 expression by siRNA
resulted in decreased expression of
Syk ... Overexpression of
c-Jun but not Ets2
resulted in increase in
Syk protein ... In conclusion,
c-Jun in cooperation with Ets2
increases the expression of
Syk and contributes to Syk mediated heightened calcium responses in SLE T cells
Koo et al., Cell Biol Int 2013
:
MPA and
Syk inhibitor
attenuated TNF-a induced DNA binding activity of NF-?B and
AP-1
Miranti et al., Curr Biol 1998
:
Additionally,
Syk and Vav1 cooperatively
induced activation of
Jun N-terminal kinase (JNK) , extracellular-signal regulated kinase 2 ( ERK2 ) and the kinase Akt, and phosphorylation of the oncoprotein Cbl in fibrinogen-adherent cells