Gene interactions and pathways from curated databases and text-mining

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CSF2 — STAT3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Yamaguchi et al., J Biol Chem 1999 : GM-CSF inhibits the nuclear translocation of tyrosine phosphorylated STAT3 ... Notably, in the presence of GM-CSF , G-CSF induced the tyrosine phosphorylation of STAT3 but failed to induce the nuclear translocation of tyrosine phosphorylated STAT3 ... Furthermore, GM-CSF caused the rapid serine727 phosphorylation of STAT3 , both in the presence and absence of G-CSF
Yang et al., Blood 1999 : In addition, hG-CSF induced phosphorylation of STAT3 but not Jak2 or STAT5, while TPO induced phosphorylation of both
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
Senis et al., Mol Cell Biol 1999 : Tyrosine phosphorylation of Stat3 and Stat5A in bone marrow derived macrophages was dramatically reduced in response to GM-CSF but not to IL-3 or IL-6
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
Sangrar et al., Exp Hematol 2003 : A molecular analysis of signaling in mature monocytic cells showed that MFps promoted GM-CSF induced STAT3 , STAT5, and ERK1/2 activation
van de Geijn et al., Blood 2004 (Disease Models, Animal...) : SOCS3 efficiently suppressed STAT3 and STAT5 activation by WT G-CSF-R in luciferase reporter assays
Stout et al., J Immunol 2004 : IL-5 and granulocyte-macrophage colony stimulating factor activate STAT3 and STAT5 and promote Pim-1 and cyclin D3 protein expression in human eosinophils
Suh et al., J Immunol 2005 : GM-CSF induced phosphorylation of Jak2, Stat5, Hck ( the myeloid restricted Src kinase ), Akt, Stat3 , and Erk MAPKs in microglia
Shao et al., J Immunol 2006 (Leukemia, Myeloid, Acute) : Unique structural determinants for Stat3 recruitment and activation by the granulocyte colony stimulating factor receptor at phosphotyrosine ligands 704 and 744
Fortin et al., Biogerontology 2007 : GM-CSF induced a transient activation of STAT3 and STAT5 in PMN of young donors but failed to activate to the same extent these signal transducers in PMN of elderly donors
Gu et al., Exp Hematol 2007 : GM-CSF induced STAT3 and survivin expression in CD34 ( + ) cells was examined by Western blot assay
Cohen et al., Blood 2008 (Neoplasms, Experimental) : Therefore, nonoverlapping, sequential activation of STAT3 and STAT5, achievable by sequenced exposure to Flt3L plus IL-6, then GMCSF , selects for multilog expansion, programming, and DC1 polarization of tumor-competent DCs from CD34 ( pos ) cells
Nguyen-Jackson et al., Blood 2010 : Using a murine model with conditional STAT3 deletion in bone marrow, we demonstrated previously that STAT3 regulates acute G-CSF-responsive neutrophil mobilization and MIP-2 dependent neutrophil chemotaxis
Souza-Fonseca-Guimaraes et al., J Biol Chem 2013 (MAP Kinase Signaling System) : IFN-? and GM-CSF production requires NF-?B and STAT3 activation as well as Erk dependent mechanisms for IFN-? and p38 signaling for GM-CSF
Xin et al., J Biol Chem 2013 (Leukemia, Myeloid, Acute) : Recently, it has also been shown that granulocyte colony stimulating factor ( G-CSF ) -induced BV8 expression is STAT3 dependent in CD11b ( + ) Gr1 ( + ) myeloid cells
Tian et al., Blood 1994 (Leukemia, Monocytic, Acute) : Rapid activation of the STAT3 transcription factor by granulocyte colony stimulating factor
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
Boulton et al., Proc Natl Acad Sci U S A 1995 : Granulocyte colony stimulating factor , which utilizes a receptor highly related to gp130, also induces these two forms of STAT3
de Koning et al., Blood 1996 : Antiphosphotyrosine immunoblots of STAT3 immunoprecipitates showed that activation of WT G-CSF-R induced phosphorylation of STAT3 ... By using tyrosine-to-phenylalanine substitution mutants of G-CSF-R, we further show that tyrosine 704, present in a YXXQ consensus sequence shown to be essential for STAT3 binding to gp130, is not exclusively involved in the activation of STAT3 by G-CSF-R
Cao et al., Mol Cell Biol 1996 : Among them, Stat3 has 52.5 % amino acid sequence homology with Stat1 and is activated by platelet derived growth factor ( PDGF ), colony stimulating factor 1 (CSF-1) , EGF, interleukin-6, and other cytokines
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
Inoue et al., Blood 1998 (Cell Transformation, Neoplastic) : As for signal transduction mediated by G-CSF receptor (G-CSFR), Stat3alpha was constitutively activated in wild-type WT1 infected 32D cl3 in response to G-CSF , whereas, in WT1 uninfected 32D cl3, activation of Stat3alpha was only transient
Miura et al., Acta Haematol 1998 (Leukemia...) : In UT-7 cells, both GM-CSF and EPO induced the activation of Stat1 alpha, Stat3 and Stat5 ... In UT-7/GM cells, EPO activated Stat5 alone, although the activation of Stat1 alpha, Stat3 , and Stat5 was induced by GM-CSF or TPO ... In addition, GM-CSF inhibited EPO induced erythroid differentiation and concomitantly activated Stat1 alpha and Stat3 in UT-7/GM cells even in the presence of EPO
Ward et al., Blood 1999 (Neutropenia) : Although one of these ( Y704 ) has previously been shown to be involved in STAT3 activation from a truncated G-CSF-R derived from a patient with severe chronic neutropenia ( SCN ), this tyrosine is not required for STAT3 activation by the full-length G-CSF-R