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CSF2 — STAT1

Pathways - manually collected, often from reviews:

• NCI Pathway Database GMCSF-mediated signaling events: GMCSF/GMR alpha/CSF2RB/JAK2 (dodecamer) complex (CSF2RB-JAK2-CSF2-CSF2RA) → STAT1-3-active (STAT1/STAT3) (modification, activates)
  Piu et al., Oncogene 2002, Brizzi et al., J Biol Chem 1996
  Evidence: physical interaction
• NCI Pathway Database GMCSF-mediated signaling events: GMCSF/GMR alpha/CSF2RB/JAK2 (dodecamer) complex (CSF2RB-JAK2-CSF2-CSF2RA) → STAT1-3 (STAT1/STAT3) (modification, activates) Piu et al., Oncogene 2002, Brizzi et al., J Biol Chem 1996
  Evidence: physical interaction

Text-mined interactions from Literome

Cassatella et al., Blood 1999 : Whereas IFNgamma and granulocyte colony stimulating factor ( G-CSF ) are efficient inducers of STAT1 and STAT3 tyrosine phosphorylation in polymorphonuclear neutrophils ( PMN ), IL-10 fails to trigger STAT1 and STAT3 tyrosine and serine phosphorylation, therefore explaining its inability to induce the FcgammaRI expression in these cells
Duarte et al., Blood 2000 : G-CSF , but not SCF, induces the tyrosine phosphorylation of STAT1 and STAT3, transcription factors that can mediate the induction of c-fos
Epling-Burnette et al., J Immunol 2001 : We found that STAT5B, STAT1 , and STAT3 DNA binding activity was induced by GM-CSF
Ahmed et al., Leukemia & lymphoma 2001 : No constitutive activation of STATs was detected in either NeoR or BCR-ABL-U937 cells, although both IFN-gamma and GM-CSF activated STAT1 and STAT5, respectively, with similar kinetics in both NeoR and BCR-ABL-U937 cells
Bovolenta et al., Blood 2002 (Leukemia, Erythroblastic, Acute) : Human T-cell leukemia virus type 2 induces survival and proliferation of CD34 ( + ) TF-1 cells through activation of STAT1 and STAT5 by secretion of interferon-gamma and granulocyte macrophage-colony stimulating factor
Jackson et al., J Immunol 2004 : Furthermore, optimal activation of STAT1 during DC maturation requires both IL-4 and GM-CSF , suggesting that synergistic effects of both cytokines may in part provide the requisite STAT1 signaling intensity for DC maturation
Kasper et al., J Interferon Cytokine Res 2007 : GM-CSF inhibited IFN-alpha induced and IFN-gamma induced Stat1 tyrosine phosphorylation in a time dependent manner
Young et al., J Immunol 2012 (Toxoplasmosis) : Although in vitro suppression of GM-CSF by IL-27 was independent of IL-2 suppression, IL-10 upregulation, or SOCS3 signaling, we observed that IL-27-driven suppression of GM-CSF was STAT1 dependent
Novak et al., Blood 1995 : Colony stimulating factor 1 (CSF-1) causes the activation of STAT1 and STAT3 transcription factors in bone marrow macrophages ( BMM ), in the macrophage cell line BAC1.2F5, and in fibroblasts that express the wild-type receptor for CSF-1
Rajotte et al., Blood 1996 : Our data indicate that GM-CSF induced DNA binding of both STAT1 and STAT3 in NIH-GMR and mainly of STAT3 in TF-1 cells
Kirito et al., J Biol Chem 1997 : This indicates that IL-3, GM-CSF , and EPO commonly activated Stat1alpha , Stat3, and Stat5 proteins in UT-7 ... Thus, although Stat1alpha , Stat3, and Stat5 proteins are activated by GM-CSF , IL-3, and EPO, our data suggest that each STAT protein has a distinctive role in the actions of cytokines
Welte et al., Eur J Immunol 1997 : Granulocyte-macrophage colony stimulating factor ( GM-CSF ) simultaneously induced complexes containing STAT1 , STAT3, STAT5A, STAT5B and STAT6
Al-Shami et al., J Biol Chem 1998 : Furthermore, GM-CSF induced the tyrosine phosphorylation of STAT3 and STAT5 but not of STAT1 , STAT2, STAT4, or STAT6