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CSF2 — JUN

Pathways - manually collected, often from reviews:

• NCI Pathway Database Calcineurin-regulated NFAT-dependent transcription in lymphocytes: JUN/FOS/NFAT1-c-4 complex (FOS-JUN-NFATC1_NFATC2_NFATC3) → GM-CSF (CSF2) (transcription, activates) Cockerill et al., Mol Cell Biol 1995, Tokumitsu et al., Biochem Biophys Res Commun 1993
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Calcium signaling in the CD4+ TCR pathway: JUN/FOS/NFAT1-c-4 complex (FOS-JUN-NFATC1_NFATC2_NFATC3) → GM-CSF (CSF2) (transcription, activates) Cockerill et al., Mol Cell Biol 1995, Tokumitsu et al., Biochem Biophys Res Commun 1993
  Evidence: mutant phenotype, physical interaction

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

Studies that report less than 10 interactions are marked with *

• IRef Innatedb Interaction: CSF2 — JUN (unknown, -) Thomas et al., Oncogene 1997*

Text-mined interactions from Literome

Seppänen et al., Oncol Res 1998 (Adenocarcinoma...) : In the present study, we have investigated the effects of interferons-alpha (IFN-alpha) and -gamma ( IFN-gamma ), interleukin-10 (IL-10) and -13 ( IL-13 ), transforming growth factor-beta1 ( TGF-beta1 ), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and tumor necrosis factor-alpha (TNF-alpha) on cell proliferation and induction of transcription factors AP-1 and NF-kappaB in UM-EC-3 human endometrial adenocarcinoma cells and UT-OC-5 ovarian carcinoma cells in vitro
Greiber et al., J Am Soc Nephrol 2002 : Activation of the transcription factor nuclear factor-kappaB (NF-kappaB) but not activator protein-1 was involved in the upregulation of ROS induced GM-CSF production
Lendemans et al., J Endotoxin Res 2006 : In contrast, the broad-spectrum tyrosine kinase inhibitor genistein and the MEK-1 inhibitor ( PD98059 ) abrogated GM-CSF priming of TNF-alpha release and activation of both NF-kappaB and AP-1
Adunyah et al., J Biol Chem 1991 : We find that GM-CSF stimulates a 2-3-fold increase in chloramphenicol acetyltransferase activity over a concentration range 1-1,000 units/ml. Northern and Western blot analysis demonstrates that the mechanism by which GM-CSF stimulates AP-1 enhancer activity involves increases in c-jun and c-fos mRNA levels, and increases in Jun protein ... These data suggest that the binding of GM-CSF to its receptor stimulates increases in c-jun mRNA and protein and activates AP-1 enhancer activity
Mascia et al., J Invest Dermatol 2010 (Dermatitis, Atopic...) : Furthermore, EGFR activation enhanced TNF-alpha induced c-Jun phosphorylation and DNA binding, whereas c-Jun silencing reduced GM-CSF expression
Ye et al., Mol Cell Biol 1996 : Taken together, these data support the ideas that AP1 and the Sp1 related nuclear protein are required for transactivation of the human GM-CSF gene promoter and that YY1 can suppress transactivation of the promoter even under inducible conditions
Tseng et al., Am J Chin Med 1996 : Si-Jun-Zi-Tang showed a suppressive effect on GM-CSF secretion at 3 hours but significantly augmented GM-CSF secretion when the cells were treated with 8 mg/ml of the drug for 18 hours