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CSF1 — FOS
Text-mined interactions from Literome
Hohensinner et al., Journal of thrombosis and haemostasis : JTH 2007
:
To determine a possible
role of nuclear factor kappaB (NF-kappaB) and
activating protein 1 (AP-1) in
M-CSF regulation, blockers to both pathways and an adenovirus overexpressing a dominant negative ( dn ) form of IkappaB kinase 2 (IKK2) were used
Chen et al., Hum Immunol 2008
:
L-selectin ligation induced
CSF-1 gene transcription is
regulated by
AP-1 in a c-Abl kinase dependent manner
Jack et al., Blood 2009
(MAP Kinase Signaling System) :
G-CSF specifically activated signal transducer and activator of transcription 3 and induced Src homology region 2 domain containing phosphatase 2 ( SHP2 ) phosphorylation, whereas
M-CSF preferentially
activated phospholipase Cgamma2, and thereby extracellular signal regulated kinase ( ERK ), to stabilize
c-Fos and stimulate CCAAT/enhancer binding protein ( C/EBP)alpha(S21 ) phosphorylation ... Inhibition of ERK prevented
induction of
c-Fos by
M-CSF and reduced C/EBPalpha phosphorylation and formation of colony forming unit-monocytes ... In summary,
M-CSF activates ERK more potently than G-CSF, and thereby induces higher levels of
c-Fos and phospho-C/EBPalpha ( S21 ), which may directly interact to favor monopoiesis, whereas G-CSF activates signal transducer and activator of transcription 3 and SHP2, potentially shifting the balance to granulopoiesis via gene induction by C/EBPalpha homodimers and via effects of SHP2 on regulators besides ERK