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JAK2 — STAT2

Pathways - manually collected, often from reviews:

• KEGG Jak-STAT signaling pathway: JAK1/JAK2/JAK3/TYK2 → STAT1/STAT2/STAT3/STAT4/STAT5A/STAT5B/STAT6 (protein-protein, phosphorylation)
  
• KEGG Chemokine signaling pathway: JAK2/JAK3 → STAT1/STAT2/STAT3/STAT5B (protein-protein, activation)
• NCI Pathway Database CXCR4-mediated signaling events: SDF1/CXCR4/JAK2 complex (CXCL12-CXCR4-JAK2) → STAT2 (STAT2) (modification, activates) Vila-Coro et al., FASEB J 1999, Zhang et al., Blood 2001
  Evidence: assay, physical interaction
• NCI Pathway Database IL27-mediated signaling events: STAT2 (STAT2) → IL27/IL27R/JAK2/TYK2 complex (IL27RA-JAK2-IL6ST-TYK2-IL27-EBI3) (modification, collaborate)
  
• WikiPathways Chemokine signaling pathway: JAK2/JAK3 → STAT1/STAT2/STAT3/STAT5B (activation)

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

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: JAK2 — STAT2 (in vivo) Marrero et al., Nature 1995*

Text-mined interactions from Literome

Velichko et al., J Biol Chem 2002 : The role of STAT1 and STAT2 in IFN dependent JAK-STAT signaling is well established ; however, the role of STAT3 and its activation by IFNs remains unclear
Hazari et al., Virology journal 2007 : All the cell lines show defect in the JAK-STAT signaling and phosphorylation of STAT 1 and STAT 2 proteins were strongly inhibited due to reduced expression of Tyk2 and Jak-1 protein
Simmons et al., J Virol 2009 : Furthermore, at times when STAT1 activation was efficiently inhibited, VRP infection did not limit tyrosine phosphorylation of Jak1, Tyk2, or STAT2 after IFN-beta treatment but did inhibit Jak1 and Jak2 activation in response to IFN-gamma, suggesting that VEEV interferes with STAT1 activation by the type I and II receptor complexes through distinct mechanisms