Gene interactions and pathways from curated databases and text-mining

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IL10RA — STAT3

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: STAT3 → IL10RA (increases, IL10RA Activity, STAT3 Activity) Crepaldi et al., J Immunol 2001*
    Evidence: The ability of IL-10 to activate Stat3 tyrosine phosphorylation and SOCS-3 synthesis and to regulate IL-1 receptor antagonist and macrophage-inflammatory protein 1beta release in LPS-treated neutrophils correlated with this increased IL-10R1 expression, and was abolished by neutralizing anti-IL-10R1 and anti-IL-10R2 Abs.
  • BioCarta il22 soluble receptor signaling pathway: STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B) → IL-22/IL-22R1/IL-22/IL-22/IL-10R2C/TYK2/JAK1/JAK1/IL-22/IL-22R1/IL-22/IL-22/IL-10R2C/TYK2/IL-22/IL-22 complex (IL22-IL22RA1-IL10RA-TYK2-JAK1) (modification, collaborate)
  • BioCarta il22 soluble receptor signaling pathway: IL-22/IL-22R1/IL-22/IL-22/IL-10R2C/TYK2/JAK1/JAK1/IL-22/IL-22R1/IL-22/IL-22/IL-10R2C/TYK2/IL-22/IL-22 complex (IL22-IL22RA1-IL10RA-TYK2-JAK1) → STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B) (modification, activates)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Ding et al., J Immunol 2003 : Induction of SOCS molecules is dependent on STAT3 activation by IL-10R1
King et al., J Surg Res 2013 : The effects of IL-10R1 signal blockade by a neutralizing antibody and STAT3 inhibition were evaluated ... Inhibition of IL-10R1 signaling results in decreased phosphorylated STAT3 levels and inhibition of nuclear localization