Figure 7

Schematic model of signaling events to MEKs and Erks induced by threshold concentrations of Epo. This basic Epo signal can be amplified or modulated by various other signaling pathways (not shown here) which become activated upon higher Epo concentrations and/or other factors and will often depend on SH2 domain interactions with the phosphorylated tyrosines in the cytoplasmic EpoR tail. PKCs could function as signal transducers for PI3Kγ, but it is also possible that PKCs are activated in a parallel pathway to PI3Kγ and that these two pathways converge to activate MEKs. B-Raf kinase does not significantly promote MAPK activation at low Epo concentrations, but since it is readily activated, it could play a role in signaling events induced by higher Epo concentrations.