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CEBPA — CSF1
Text-mined interactions from Literome
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 ... 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
Zhang et al., Mol Cell Biol 1996
:
Further transfection studies show that
C/EBP and AML1 in concert with the AML1 heterodimer partner CBF beta synergistically
activate M-CSF receptor by more then 60 fold
Petrovick et al., Mol Cell Biol 1998
:
We have shown that AML1 and
C/EBPalpha activate the
M-CSF receptor promoter in a synergistic manner