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CSF3 — MAPK6

Text-mined interactions from Literome

Yamaguchi et al., J Biol Chem 1999 : G-CSF caused the activation of p70 S6 kinase but not mitogen activated protein ( MAP ) kinase
Srinivasa et al., Leukemia 2002 (Leukemia, Monocytic, Acute...) : Both G-CSF and FL induced phosphorylation of extracellular signal regulated kinases ( ERKs ) while p38 mitogen activated protein ( MAP ) kinase was phosphorylated only in response to G-CSF but not FL. Studies using specific kinase inhibitors suggested that both ERK and p38 MAP kinase pathways were required for the optimal cell proliferation in response to both G-CSF and FL
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
Kimura et al., J Biol Chem 2004 (MAP Kinase Signaling System) : Consistent with this notion, G-CSF induced STAT3 as well as mitogen activated protein kinase activation was much stronger and prolonged in SOCS3-deficient mature neutrophils than in wild-type neutrophils
Fusté et al., Haematologica 2004 : Granulocyte colony stimulating factor increases expression of adhesion receptors on endothelial cells through activation of p38 MAPK
Baumann et al., Leuk Res 2005 : Although both GM-CSF and G-CSF activate p42/44 MAPK in neutrophil progenitors, the ability of G-CSF to cause MAPK activation is lost in mature neutrophils, while GM-CSF exposure still causes activation
Uemura et al., Int J Mol Med 2005 (Lung Neoplasms) : The induction of G-CSF expression via PKC inhibition was mediated by p44/42 mitogen activated protein kinase and c-Jun N-terminal kinase pathway signaling
Uemura et al., Int J Lab Hematol 2009 (Leukemia, Neutrophilic, Chronic) : We also showed that stat3 and mitogen activated protein kinase activation by G-CSF or GM-CSF in the patient 's neutrophils were significantly lower than those in healthy donor neutrophils
Liu et al., Invest Ophthalmol Vis Sci 2008 : Poly ( I:C ) -induced expression of IL-6, IL-8, G-CSF , MIP-1beta, exotaxin, RANTES, and ICAM-1 was inhibited differentially by the MAPK inhibitors PD98059 and SB203580 and by JNK inhibitor II
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