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CSF2 — EPHB2

Text-mined interactions from Literome

Iida et al., Leukemia 1999 (Acute Disease...) : Three samples with N-Ras mutations were stimulated with IL-3, GM-CSF and G-CSF separately but ERK2 activation was induced in none of these samples stimulated with these cytokines
Yagisawa et al., Exp Hematol 1999 : In marked contrast to neutrophils and MO7e cells, GM-CSF did not induce tyrosine phosphorylation and activation of ERK in monocytes
Valledor et al., J Biol Chem 2000 : Granulocyte/macrophage colony stimulating factor , interleukin 3, and TPA, all of which induced macrophage proliferation, also induced ERK activity, which was maximal at 5 min poststimulation
Lee et al., Biochem Biophys Res Commun 2001 : p44/42 MAP kinase (ERK1/2) was synergistically activated by SLF plus GM-CSF , but SAPK/JNK and p38 MAP kinase were not
Hallsworth et al., Am J Respir Crit Care Med 2001 (Asthma...) : GM-CSF release is p42/p44 ERK dependent and is tonically suppressed by a mechanism that is partially dependent on p38 MAP kinase, though direct inhibition of cyclooxygenase (COX) activity due to poor inhibitor selectivity may also contribute
Kolonics et al., Haematologia (Budap) 2001 (Acute Disease...) : In UCBMNC and NBMMNC, Epo and GM-CSF induced the activation of STAT-5 DNA binding and ERK 1/2 activation ( n = 6 )
Okuma et al., Exp Hematol 2002 (MAP Kinase Signaling System) : Transient phosphorylation and activation of ERK was induced by both GM-CSF alone and combination of the two cytokines, whereas sustained phosphorylation and activation was induced only by the combination
Bozinovski et al., J Biol Chem 2002 (MAP Kinase Signaling System) : Pharmacological inhibition of Akt or Erk activation in LPS treated tracheal explants ex vivo inhibited the release of GM-CSF
Rolli-Derkinderen et al., J Biol Chem 2003 : PMA and granulocyte/macrophage colony stimulating factor induce Egr-1 expression through ERK and p38 activation, respectively
Li et al., Biochem Biophys Res Commun 2003 : Immunoblotting studies show that GM-CSF alone induced ERK2 phosphorylation ; whereas, IL-10 alone induced p70 ( S6k ) phosphorylation in U937 cells
Kutsuna et al., Am J Physiol Cell Physiol 2004 : These findings suggest that TNF, GM-CSF , and G-CSF induce actin depolymerization and morphological changes through activation of ERK and/or p38 MAPK and that cytokine induced actin reorganization may be partly responsible for the inhibitory effect of these cytokines on neutrophil chemotaxis
Zhou et al., J Biol Chem 2003 : IFNgamma induced MMP-1 in the presence of GM-CSF through the stimulation of TNFalpha production through a mechanism involving both p38 and ERK1/2 MAPKs, in which GM-CSF stimulated ERK1/2 whereas IFNgamma activated p38
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
Murata-Ohsawa et al., Int J Mol Med 2004 (MAP Kinase Signaling System) : GM-CSF stimulation induced the phosphorylation of ERK1/2 and STAT5 and the cleavage of caspase-8, which were not affected by Delta-1 incubation, either
Bowdish et al., J Immunol 2004 (MAP Kinase Signaling System) : Activation of ERK1/2 and p38 was markedly increased by the presence of GM-CSF , but not M-CSF
Zheng et al., Leukemia 2004 (Leukemia, Erythroblastic, Acute...) : Further, HQ and rhGM-CSF together produce an immediate increase in ERK phosphorylation, which is sustained for over 48 h. HQ also stimulates colony formation, AP-1 DNA binding and GM-CSF production in human CD34+ BM cells
Patel et al., J Biol Chem 2006 (Inflammation...) : Exposure to apoptotic cells led to nearly complete inhibition of both basal and macrophage colony stimulating factor induced ERK1/2 by macrophages
Derouet et al., J Immunol 2006 : For example, sodium salicylate blocked GM-CSF stimulated Erk and Akt activation, but resulted in rapid and sustained activation of p38-MAPK, an event mimicked by okadaic acid that also accelerates Mcl-1 turnover and neutrophil apoptosis
Matsubara et al., Int Arch Allergy Immunol 2006 : Ro-31-8220, a PKC inhibitor, and PD98059, a mitogen activated protein/ERK kinase inhibitor, suppressed the histamine induced ERK activation and the production of granulocyte macrophage colony stimulating factor and IL-8
Dang et al., FASEB J 2006 : We found that IL-10 inhibited GM-CSF induced ERK1/2 activity in an immunocomplex kinase assay
Yano et al., Atherosclerosis 2007 : We previously reported that oxidized low-density lipoprotein ( Ox-LDL ) induces macrophage proliferation through ERK1/2 dependent GM-CSF production ... In conclusion, troglitazone inhibited Ox-LDL induced GM-CSF production by suppressing nuclear translocation of ERK1/2 , thereby inhibiting macrophage proliferation
Tortorella et al., J Gerontol A Biol Sci Med Sci 2006 : Whereas Akt inhibition also affected GM-CSF dependent ERK1/2 phosphorylation, ERK1/2 inhibition did not affect GM-CSF induced Akt phosphorylation, suggesting that phosphoinositide 3-kinase (PI3-K)/Akt and ERK1/2 are activated in series and that PI3-K is located upstream of ERK1/2 along the GM-CSF dependent signaling pathway
Seo et al., Ann N Y Acad Sci 2007 : ERK signaling regulates macrophage colony stimulating factor expression induced by titanium particles in MC3T3.E1 murine calvarial preosteoblastic cells
Shima et al., Am J Hypertens 2008 : By contrast, GM-CSF induced phosphorylation of ERK , p38, and Akt was affected by none of the blockers
Fuxman Bass et al., Mol Immunol 2008 : We also found that GM-CSF enhanced the activation of the MAPKs p38 and ERK1/2 induced by bacterial DNA
Montenegro et al., Cell Prolif 2009 (Leukemia, Myeloid) : TGFbeta inhibits GM-CSF induced phosphorylation of ERK and MEK in human myeloid leukaemia cell lines via inhibition of phosphatidylinositol 3-kinase (PI3-k) ... In contrast, GM-CSF induced rapid and transient phosphorylation of MEK1/2 and ERK1/2 and up-regulated cell proliferation ... Both GM-CSF induced ERK1/2 activation and cell proliferation were significantly inhibited by TGFbeta ... PD98059, a selective inhibitor of MEK, blocked GM-CSF induced phosphorylation of MEK and ERK but not p85 ... These studies thus indicate that TGFbeta does not activate the ERK pathway but turns off the GM-CSF induced ERK signal via inhibition of the PI3-kinase-Akt pathway, in these human leukaemia cells
Chan et al., Blood 2009 (Myeloproliferative Disorders) : Ptpn11 ( D61Y ) common myeloid progenitors ( CMPs ) and granulocyte-monocyte progenitors (GMPs) produce cytokine independent colonies in a cell-autonomous manner and demonstrate elevated Erk and Stat5 activation in response to granulocyte-macrophage colony stimulating factor ( GM-CSF ) stimulation
Seo et al., Bone 2010 (MAP Kinase Signaling System...) : In the context of osteoclastogenesis, macrophage colony stimulating factor ( M-CSF ) is an upstream activator of ERK signals for the survival of osteoclast precursors prior to their differentiation into multinucleated osteoclasts
Hua et al., Int Immunopharmacol 2010 (Arthritis, Rheumatoid) : ERK activation by GM-CSF reduces effectiveness of p38 inhibitor on inhibiting TNFalpha release
Leon et al., J Cell Physiol 2011 (Calcium Signaling) : Requirement for PLC?2 in IL-3 and GM-CSF stimulated MEK/ERK phosphorylation in murine and human hematopoietic stem/progenitor cells
Gandre-Babbe et al., Blood 2013 (Leukemia, Myelomonocytic, Juvenile) : In vitro differentiation of JMML iPSCs produced myeloid cells with increased proliferative capacity, constitutive activation of granulocyte macrophage colony stimulating factor ( GM-CSF ), and enhanced STAT5/ERK phosphorylation, similar to primary JMML cells from patients
Gotoh et al., Cell Growth Differ 1997 : Erk2 and Vav were also tyrosine phosphorylated by stimulation with Steel factor ( SLF ) and granulocyte macrophage colony stimulating factor , whereas tyrosine phosphorylation of Syk was not induced by stimulation with these cytokines
Egerton et al., Int Immunol 1998 : However, the production of IL-3 and IL-4 was only partially dependent upon ERK activation, whereas IL-5, IL-10, IFN-gamma and GM-CSF production was severely affected by diminished ERK activation
McLeish et al., J Leukoc Biol 1998 : GM-CSF stimulated ERK activity comparable to that of TNF-alpha, but GM-CSF was a less potent stimulus of p38 MAPK activity
Suzuki et al., Blood 1999 : MEK inhibitor ( PD98059 ) reduced tyrosine phosphorylation of ERK , but not p38 MAPK, induced by G-CSF , GM-CSF, or TNF