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IL12B — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Nakahira et al., J Immunol 2002
:
An increase in c-Jun, a component of AP-1, in the nuclear compartment was elicited by stimulation with either
IL-12 or IL-18, but accumulation of serine phosphorylated
c-Jun was
induced only by IL-18 capable of activating c-Jun N-terminal kinase
Sugimoto et al., Eur J Immunol 2003
:
IL-18, but not
IL-12 ,
induced activator protein-1 (AP-1) responsible for high levels of IFN-gamma promoter activation
Ma et al., J Immunol 2004
:
The
role of
AP-1 in
IL-12p40 transcription was confirmed by using antisense c-fos and c-jun oligonucleotides ... Taken together, our results suggest that DXM may
inhibit IL-12p40 production in LPS stimulated human monocytic cells by down regulating the activation of JNK MAPK, the
AP-1 , and NF-kappaB transcription factors
Park et al., Int Immunol 2004
:
IL-12 stimulation greatly
enhanced the promoter binding activity of
c-Jun/AP-1 , a critical transcription factor for IFN-gamma gene expression in wild-type T cells, but not in STAT4-deficient ( STAT4 ( -/- ) ) T cells ...
IL-12 stimulation greatly
enhanced the promoter binding activity of
c-Jun/AP-1 , a critical transcription factor for IFN-gamma gene expression in wild-type T cells, but not in STAT4-deficient ( STAT4 ( -/- ) ) T cells
Matsumoto et al., J Immunol 2004
(Inflammation) :
Concomitantly, simvastatin induces the phosphorylation of c-Jun by the c-Jun N-terminal kinase, resulting in
c-Jun dependent activation of the
IL-12p40 promoter
Ma et al., J Biol Chem 2009
(Acquired Immunodeficiency Syndrome) :
We have previously shown that lipopolysaccharide (LPS) induced
IL-12p40 production in monocytic cells is
regulated by NFkappaB and
AP-1 transcription factors through the activation of two distinct upstream signaling pathways, namely the c-Jun-N-terminal kinase (JNK) and the calmodulin dependent protein kinase-II activated pathways
Wang et al., J Immunol 2012
:
ESAT-6 reduced LPS/CD40L stimulated transcription of IL-12p35 and enhanced that of IL-23p19 through inhibition of IFN regulatory factor-1 and upregulation of activating transcription factor-2 and
c-Jun , transcriptional
regulators of
IL-12p35 and IL-23p19, respectively