Fig. 1.

JAK2 signaling. a Binding of Epo to EpoR results in receptor homodimerization and autophosphorylation (marked with P) of JAK2, which in turn mediates the phosphorylation of key tyrosine residues of EpoR, docking sites for downstream effectors, including STAT5, PI3K, and MAPK, and influencing downstream pathways involved in proliferation, differentiation, preventing apoptosis, and regulating iron metabolism. b In polycythemia vera, JAK2 mutations result in a constitutively active signaling in the absence of Epo. Epo erythropoietin, JAK2 janus kinase 2, JAK2 mut JAK2 mutation (i.e., V617F and exon 12), STAT5 signal transducer and activator of transcription 5, PI3K phosphatidylinositol 3 kinase, MAPK mitogen-activated protein kinase, ERK extracellular signal–regulated kinase, AKT serine/threonine-protein kinase B, GATA1 globin transcription factor 1, Spi2A spindlin family member 2A, ERFE erythroferrone