Identifiers
HUGO:JUN HUGO:JUNB HUGO:JUND HUGO:JBP1 HUGO:FOS HUGO:FOSB HUGO:FOSL1 HUGO:FOSL2 HUGO:MAF HUGO:MAFB HUGO:MAFA HUGO:MAFG HUGO:MAFK HUGO:MAFF HUGO:NRL HUGO:ATF1 HUGO:ATF2 HUGO:ATF3 HUGO:BATF HUGO:BATF2 HUGO:BATF3 HUGO:JDP2
Maps_Modules
HMC:AVOIDING_IMMUNE_DESTRUCTION
Adaptive Immune Response / TCR_SIGNALING
References
PMID:11148124
JNK/AP1 signaling is activated in T-cells downstream of TCR signaling
PMID:15214048; PMID:10807788; PMID:24027568
AP-1 activation by Tec is largely dependent on PLC??1 function. Moreover, ionomycin did not enhance Tec-induced AP-1 activation (Fig. 4C), also suggesting that Tec contributes to AP-1 activation upstream of Ca2+ release.
probably via RAS/ERK pathway
PMID:11262396
We examined whether Vav2 overexpression results in stimulation of c-fos SRE transcriptional activity. We transfected Jurkat-TAg cells with Myc-tagged Vav1 or Vav2 along with a luciferase reporter driven by SRE-binding sequences. Similarly both Vav1 and Vav2 induced a marked increase of either the basal or TCR-stimulated activities of SRE reporter plasmid12818166
PMID:16713974
GSK3B inhitits activation (DNA binding) of AP-1 factors.
JNK is a classical activator of AP1 transcription factors.
Inhibition of JNK downregulates IL10 expression. Probably via
AP1.
PMID:9743347
IL13 inhibits JNK phosphorylation and AP1 activation (provavly via dusp1)
PMID:9064320
CD16-induced ERK activation provides TNFA expression in NK cells.
MEK/ERK cascade induces AP1(c-fos) phosphorylation downstream of CD16 (
PMID:23681101, PMID:11477091
There are three main signaling pathways could be activated downstream of TRR4/MyD88/TAK1 signaling??: p38 (via MKK3 or MKK6), JNK (via MKK4 or MKK7) and NfkB ) IN DC all these signaling pathways are activated downstream of TLR4 and TLR2 signaling )
PMID:11438547, PMID:24378531
in macrophages
Both TNFR1 and TNFR2 signaling pathways induce classical NFkB activation via IKBa degradation.
Both TNFR1 and TNFR2 signaling pathways induce JNK activation and downstrean c-jun phosphorylation.
Both TNFR1 and TNFR2 signaling pathways are needed for activation of p38 MAPK.
PMID:16327802
IL13 and TNF inducese TGFB1 expression via AP-1 transcription factors.IL13 induces binding of c-jun and fra2 ti TGFB1 promotor, and TNF binding of c-jun, JunD and c-fos.
References
in_re1149( Innate Immunity ):
PMID:16713974
GSK3B inhitits activation (DNA binding) of AP-1 factors.
JNK is a classical activator of AP1 transcription factors.
Inhibition of JNK downregulates IL10 expression. Probably via
AP1.
References
in_re1149( Innate Immunity ):
PMID:16713974
GSK3B inhitits activation (DNA binding) of AP-1 factors.
JNK is a classical activator of AP1 transcription factors.
Inhibition of JNK downregulates IL10 expression. Probably via
AP1.
in_re1364( Innate Immunity ):
PMID:16327802
IL13 and TNF together (but neither IL-13 nor TNF alone) upregulates TGFB1 expression downstream of IL13RA2.
IL13 and TNF inducese TGFB1 expression via AP-1 transcription factors.IL13 induces binding of c-jun and fra2 ti TGFB1 promotor, and TNF binding of c-jun, JunD and c-fos.
PMID:21372296
HMGB1 markedly increased the expression of the genes for VEGF, and TGFB1 in
peritoneal macrophages via TLR4-dependent mechanisms.