JNK*

Protein JNK*

Identifiers
HUGO:MAPK8 HGNC:6881 ENTREZ:5599 UNIPROT:P45983 GENECARDS:MAPK8 HUGO:MAPK9 HGNC:6886 ENTREZ:5601 UNIPROT:P45984 GENECARDS:MAPK9 HUGO:MAPK10 HGNC:6872 ENTREZ:5602 UNIPROT:P53779 GENECARDS:MAPK10

Maps_Modules
MODULE:CORE_SIGNALING_PATHWAYS MODULE:IMMUNOSTIMULATORY_CORE_PATHWAYS

References
REACTOME:59293 KEGG:5599 ATLASONC:JNK1ID196 WIKI:MAPK8
mitogen-activated protein kinase 9
REACTOME:59295 KEGG:5601 ATLASONC:JNK2ID426 WIKI:MAPK9
mitogen-activated protein kinase 10
REACTOME:59297 KEGG:5602 ATLASONC:JNK3ID427 WIKI:MAPK10
MACROPHAGE
NATURAL_KILLER
CASCADE:IL10
CASCADE:TLR2_4
CASCADE:IL18
CASCADE:NKG2D
CASCADE:TNF
CASCADE:IFNG
PMID:18287025
JNK is localized to the centrosome.
JNK induces assosiation of Paxilin with MTOC resulted in polarization of the MTOC
and cytolytic granules, and finally exocytosis of cytolytic proteins downstream of NKG2D.
Inhibition of JNK activity by D-JNK-1, SP600125, Or JNK-1-specific siRNA blocked polarization of granzyme B,
PMID:17070508
IL-2/IL-18 prevent the down-modulation of NKG2D by TGF-beta in NK cells via the c-Jun N-terminal kinase (JNK) pathway.
PMID:10465784
ECSIT (evolutionarilyconserved signaling intermediate inToll pathways), is specific for the Toll/IL-1 pathways and is a regulator of MEKK-1 processing. Expression of wild-type ECSIT accelerates processing of MEKK-1, whereas a dominant-negative fragment of ECSIT blocks MEKK-1 processing and activation of NF-κB
ECSIT mutant also strongly inhibited MEKK-1 activation of AP-1 (probably via MAP2K4/JNK),
additionally TRAF6-induced signaling is inhibited by dominant-negative constructs of MEKK-1.
PMID:17379190
MEK4/JNK/AP-1 path way is active in mactophages downstream of TLR4,
and induces iNOS expression.
PMID:16243976
IRF4 downregulates expression of TNFa, IL12p40, IL6 probably via inhibition of NF-kB and JNK signaling pathways.
PMID:17073741
DUSP1 inhibits p38 and JNK pathways of innate innunity downstream of IL10.
PMID:9743347
IL13 inhibits JNK phosphorylation and AP1 activation (provavly via dusp1)
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:23508573
HMGB1 induces activation (phosphorylation) of ERK, JNK and p38 via TLR4 in macrophages.
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:16713974, PMID:11579131
INFG pathway inhibits activation (phosphorylation) of ERK, JNK, p38 kinases and PI3K pathway induced by TLR. Inhibition of AKT pathway by IFNG resulted in activation of GSK3. GSK3 inhibits downstream AP-1 and CREB1 signaling and downregulates IL10 expression induced by TLR.IFNG inhibits CREB activation via p38 induced by TLR signaling

JNK*@INNATE_IMMUNE_CELL_Cytosol

References
PMID:16713974
TLR2 activates (induses phosphorylation of) ERKs, JNKs, and p38 rapidly and transiently in control macrophages.

Modifications:
In compartment: INNATE_IMMUNE_CELL_Cytosol

JNK*@INNATE_IMMUNE_CELL_Cytosol
JNK*|pho|active@INNATE_IMMUNE_CELL_Cytosol

Participates in complexes:

Participates in reactions:
As Reactant or Product:

JNK*@INNATE_IMMUNE_CELL_Cytosol → JNK*|pho|active@INNATE_IMMUNE_CELL_Cytosol

As Catalyser: