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FOS — STAT3

Pathways - manually collected, often from reviews:

• FastForward regulation: STAT3 → FOS (transcriptional regulation, unknown) Ehret et al., J Biol Chem 2001*, Murai et al., Mol Cell Biol 2002, Schreiner et al., J Biol Chem 2002, Yang et al., J Biol Chem 2003*
  Evidence: DNABINDING
• NCI Pathway Database IL6-mediated signaling events: STAT3 (dimer ) complex (STAT3) → AP1 complex (FOS-JUN) (transcription, activates) Schumann et al., Mol Cell Biol 1996*
  Evidence: mutant phenotype, reporter gene, physical interaction
• NCI Pathway Database IL6-mediated signaling events: STAT3 (dimer ) complex (STAT3) → AP1 complex (FOS-JUN) (transcription, activates) Bugno et al., Nucleic Acids Res 1995*
  Evidence: mutant phenotype, physical interaction, other species

Text-mined interactions from Literome

Higashi et al., Genes Cells 2004 (MAP Kinase Signaling System) : Cytoplasmic c-Fos induced by the YXXQ derived STAT3 signal requires the co-operative MEK/ERK signal for its nuclear translocation ... Activation of a truncated form of the IL-6 receptor subunit, gp130, that had only one YXXQ motif, induced both c-Fos and JunB in NIH3T3 cells through STAT3 without an apparent increase in the AP-1 ( activator protein-1 ) activity ... In contrast, concomitant stimulation of the STAT3 signal and a MEK/Erk-signal markedly increased AP-1 activity with enhanced c-Fos expression ... In contrast, concomitant stimulation of the STAT3 signal and a MEK/Erk-signal markedly increased AP-1 activity with enhanced c-Fos expression ... Thus, the YXXQ-signal induces c-Fos expression through STAT3 and anchors the new c-Fos in the cytoplasm
Janoschek et al., Proc Natl Acad Sci U S A 2006 (Acute Disease...) : Correspondingly, in these animals, CNTF failed to activate STAT3 phosphorylation in POMC neurons and to induce c-Fos expression in the paraventricular nucleus
Kwon et al., J Immunol 2012 : PKC-? mediated activation of the Stat3 promoter was inhibited by dominant negative AP-1 and I?B kinase-ß, but stimulated by WT AP-1 and I?B kinase-ß, suggesting that PKC-? stimulates Stat3 transcription via the AP-1 and NF-?B pathways
Wei et al., Acta Pharmacol Sin 2013 : Furthermore, the treatment selectively prevented the activation of MAPKs, AKT and transcription factor AP-1 component c-Jun, but not the recruitment of TRAF6 or the activation of JAK2/STAT3