◀ Back to STAT3

JUN — STAT3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: FAS → Complex of JUN-STAT3 (decreases)
  Evidence: Downregulation of FAS expression is a common event during tumor progression and has been correlated with resistance to radiation or drug-induced cell death. Importantly, STAT3 binds directly to the FAS promoter in association with JUN to suppress the transcription of the death receptor.
• 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

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: STAT3 — JUN (physical association, affinity chromatography technology) Zhang et al., Mol Cell Biol 1999*
• IRef Biogrid Interaction: STAT3 — JUN (direct interaction, pull down) Zhang et al., Mol Cell Biol 1999*
• IRef Hprd Interaction: STAT3 — JUN (in vitro) Zhang et al., Mol Cell Biol 1999*
• IRef Hprd Interaction: STAT3 — JUN (in vivo) Zhang et al., Mol Cell Biol 1999*
• IRef Ophid Interaction: STAT3 — JUN (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Turkson et al., Mol Cell Biol 1999 (Cell Transformation, Neoplastic...) : Requirement for Ras/Rac1 mediated p38 and c-Jun N-terminal kinase signaling in Stat3 transcriptional activity induced by the Src oncoprotein
Higashi et al., Genes Cells 2004 (MAP Kinase Signaling System) : In contrast, concomitant stimulation of the STAT3 signal and a MEK/Erk-signal markedly increased AP-1 activity with enhanced c-Fos expression
Ogunwobi et al., Int J Colorectal Dis 2007 (Colonic Neoplasms) : Activation of JAK2 was followed by activation and nuclear translocation of STAT3 and JNK activation led to increased activator protein 1 (AP-1) transcriptional activity
Gazi et al., Clin Chim Acta 2007 (Prostatic Neoplasms) : Interestingly, although sodium selenite did not show effect on activation of both STAT3 and ERK1/2 in the presence of IL-6, an increased expression of c-Jun was detected in cells after treatment with sodium selenite
Reipschläger et al., J Biol Chem 2012 : RhoA dependent STAT3 stimulation requires ROCK and Jun kinase activation as well as AP1 induced protein synthesis
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
Lu et al., J Dermatol 2013 : Importantly, JUN may regulate activating transcription factor 3 expression to involve cell proliferation process ; STAT1 and STAT3 can inhibit tissue inhibitor of metalloproteinases-3 expression to modulate the cell adhesion molecule pathway ; NF-?B and E2F1 can downregulate cyclin D1, but upregulate proliferating cell nuclear antigen expression to promote the cell cycle pathway
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