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IL23R — STAT3
Pathways - manually collected, often from reviews:
-
NCI Pathway Database IL23-mediated signaling events:
STAT3 (STAT3)
→
IL23/IL23R/JAK2/TYK2 complex (IL23A-IL12B-IL23R-IL12RB1-JAK2-TYK2)
(modification, collaborate)
Parham et al., J Immunol 2002, Cho et al., J Immunol 2006
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database IL23-mediated signaling events:
STAT3 (STAT3)
→
IL23/IL23R/JAK2/TYK2 complex (IL23A-IL12B-IL23R-IL12RB1-JAK2-TYK2)
(modification, collaborate)
Oppmann et al., Immunity 2000, Parham et al., J Immunol 2002
Evidence: assay, physical interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Huber et al., Proc Natl Acad Sci U S A 2008
:
Current dogma proposes that IL-6 induces IL-21, which, in a
STAT3 dependent manner, amplifies its own transcription, contributes to IL-17 production, and, moreover, promotes the expression of the
IL-23 receptor
Staschke et al., J Immunol 2009
(Encephalomyelitis, Autoimmune, Experimental) :
Furthermore, the absence of IRAK4 kinase activity blocked induction of
IL-23R expression,
STAT3 activation by IL-23, and Th17 cytokine expression in differentiated Th17 cells