◀ Back to MAPK10
CSF1 — MAPK10
Text-mined interactions from Literome
Liu et al., Mol Cell Biol 2001
:
Overexpression of Gab2 in FD-Fms cells enhanced both
mitogen activated protein kinase ( MAPK ) activity and macrophage differentiation, but reduced proliferation, in
response to
M-CSF
Gobert Gosse et al., Cell Signal 2005
(MAP Kinase Signaling System) :
M-CSF stimulated differentiation
requires persistent MEK activity and
MAPK phosphorylation independent of Grb2-Sos association and phosphatidylinositol 3-kinase activity ... This compound could not impede FD/Fms cell commitment to macrophage differentiation and did not significantly affect
MAPK phosphorylation in
response to
M-CSF
Gunawardane et al., Cancer Res 2005
(Breast Neoplasms...) :
Constitutive activation of the extracellular signal regulated kinase ( ERK ) pathway also enhanced PDEF induced motility and invasion, suggesting that
activation of the
ERK/mitogen activated protein kinase by ErbB2 and
CSF-1R/CSF-1 can cooperate with PDEF to promote motility and invasion
Eda et al., Rheumatol Int 2011
(MAP Kinase Signaling System) :
These results showed that proinflammatory cytokines, IL-1ß and TNF-a, induced the expression of IL-34 mRNA via JNK and p44/42
MAPK but not p38 in human osteoblasts while p38, JNK, and p44/42 MAPK were not
involved in the induction of
M-CSF mRNA expression by these cytokines
Nikolic et al., BMC immunology 2011
:
M-CSF increased SR-A expression and function, and
required the specific activation of p38
MAPK , but not ERK1/2 or JNK
Cheng et al., PloS one 2013
:
The
MCSF- and oxLDL induced proliferation of peritoneal macrophages from GPx-1 ( -/- ) ApoE ( -/- ) mice was
mediated by the p44/42
MAPK ( p44/42 mitogen activated protein kinase ), namely ERK1/2 ( extracellular-signal regulated kinase 1/2 ), signaling pathway as demonstrated by ERK1/2 signaling pathways inhibitors, Western blots on cell lysates with primary antibodies against total and phosphorylated ERK1/2, MEK1/2 ( mitogen activated protein kinase kinase 1/2 ), p90RSK ( p90 ribosomal s6 kinase ), p38 MAPK and SAPK/JNK ( stress activated protein kinase/c-Jun N-terminal kinase ), and immunohistochemistry of mice atherosclerotic lesions with antibodies against phosphorylated ERK1/2, MEK1/2 and p90RSK
Büscher et al., Mol Cell Biol 1995
:
Expression of a dominant negative ras mutant reduced, but did not abolish,
CSF-1 mediated stimulation of MEK and
MAPK ... Similarly, down-regulation or inhibition of protein kinase C blocked MEK and
MAPK induction by LPS but not that by
CSF-1
Qiu et al., J Biol Chem 1998
:
CSF-1 is a strong
MAPK activator that induces a rapid and complete cPLA2 gel shift but not calcium mobilization or arachidonic acid release
Hatch et al., Blood 1998
(Leukemia, Monocytic, Acute) :
Inhibition of RAFTK by a dominant negative kinase mutant reduced
CSF-1/M-CSF induced
MAPK activity
Fowles et al., Mol Cell Biol 1998
:
Kinase assays that used recombinant ets-2 protein as a substrate demonstrated that
mitogen activated protein ( MAP ) kinases p42 and p44 were constitutively activated in both cell types in
response to
CSF-1