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AKT2 — 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
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