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CSF3 — MAPK7
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