Gene interactions and pathways from curated databases and text-mining

◀ Back to CSF1

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