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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 *

• IRef Hprd Interaction: STAT3 — IL23R (in vivo) Parham et al., J Immunol 2002
• IRef Hprd Interaction: STAT3 — IL23R (in vitro) Parham et al., J Immunol 2002

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