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AKT1 — CSF2

Text-mined interactions from Literome

Miike et al., J Leukoc Biol 1999 : However, neither two PI-3 kinase inhibitors, wortmannin and LY294002, nor MEK inhibitor PD98059 inhibited GM-CSF induced survival of eosinophils, although wortmannin and PD98059 inhibited GM-CSF induced Akt phosphorylation and MAP kinase activation in eosinophils, respectively
Kelley et al., J Biol Chem 1999 : To clarify that PI3K products activate Akt in response to M-CSF , NIH 3T3 fibroblasts expressing mutant human M-CSF receptors ( 3T3-FMS ( Y809F ) ) that fail to activate Ras in response to M-CSF also exhibit increased Akt kinase activity in response to M-CSF challenge
Liu et al., Mol Biol Cell 1999 : GM-CSF activates phosphoinositide-3-OH kinase as well as Akt , and activation of both was suppressed by addition of wortmannin
Zocchi et al., Eur J Immunol 2001 (Leukemia, Myeloid, Acute) : Leukocyte associated Ig-like receptor-1 prevents granulocyte-monocyte colony stimulating factor dependent proliferation and Akt1/PKB alpha activation in primary acute myeloid leukemia cells
Bozinovski et al., J Biol Chem 2002 (MAP Kinase Signaling System) : LPS markedly activated Akt and Erk1/2, but not p38, in a GM-CSF dependent manner in direct temporal association with NFkappaB and AP-1 activation ... Pharmacological inhibition of Akt or Erk activation in LPS treated tracheal explants ex vivo inhibited the release of GM-CSF ... These data implicate GM-CSF dependent activation of Akt in the amplification of this response and demonstrate the role of Erks rather than p38 in lung LPS inflammatory responses
Yasui et al., J Leukoc Biol 2002 : In addition, no major GM-CSF dependent delay in apoptosis or activation of Akt protein phosphorylation by GM-CSF was observed in the p85alpha-/- mice
Baran et al., J Biol Chem 2003 : The inositol 5'-phosphatase SHIP-1 and the Src kinase Lyn negatively regulate macrophage colony stimulating factor induced Akt activity ... These data provide the first evidence of the involvement of both SHIP-1 and Lyn in the negative regulation of M-CSF-R induced Akt activation
Senokuchi et al., Atherosclerosis 2004 (Arteriosclerosis...) : Recombinant GM-CSF induced PI-3K activation and Akt phosphorylation were significantly inhibited by SB203580 but enhanced by PD98059
Kamata et al., Int J Hematol 2004 : Stimulation of human neutrophils with granulocyte colony stimulating factor ( G-CSF ), granulocyte-macrophage CSF (GM-CSF) , or tumor necrosis factor alpha (TNF) resulted in phosphorylation of Akt , the potency being GM-CSF > G-CSF = TNF, which was inhibited by wortmannin
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
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
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
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
Ishii et al., J Biol Chem 2009 : AICAR suppressed GM-CSF induced macrophage proliferation without suppressing p38 MAPK/Akt signaling
Bergmann et al., Hypertension 2010 : Aldosterone had no effect on tumor necrosis factor alpha- and lipopolysaccharide mediated nuclear factor kappaB activation or on IL-8- and granulocyte/macrophage colony stimulating factor induced extracellular signal regulated kinase, p38 mitogen activated protein kinase, or phosphatidylinositol 3-kinase/Akt activation
Liontos et al., J Immunol 2011 : In bone marrow derived DC ( BM-DC ) lacking SLAP and the closely related SLAP2, downregulation of GM-CSFRß is impaired, leading to enhanced phosphorylation of Jak2 and prolonged activation of Akt and Erk1/2 in response to GM-CSF stimulation