Gene interactions and pathways from curated databases and text-mining

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CSF1 — MAPK7

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