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Molecular mechanisms of thrombopoietin signaling Kaushansky KJ Thromb Haemost 2009[Jul]; 7 Suppl 1 (ä): 235-8The molecular pathways that regulate thrombopoiesis are becoming increasingly understood. Upon binding to its receptor, the product of the c-Mpl proto-oncogene, thrombopoietin activates a number of secondary messengers that promote cell survival, proliferation and differentiation. Amongst the best studied are the signal transducers and activators of transcription, phosphoinositol-3-kinase, and the mitogen-activated protein kinases. Additional signals activated by these secondary mediators include mammalian target of rapamycin, beta-catenin, hypoxia-inducible factor 1alpha and the homeobox proteins HOXB4 and HOXA9, and a number that are reduced, including glycogen synthase kinase 3alpha and the FOXO3 family of forkhead proteins. More recently, a number of signaling pathways have been identified that turn the thrombopoietin signal off, a step necessary to avoid uncontrolled myeloproliferation, and include the phosphatases PTEN, SHP1 and SHIP1, the suppressors of cytokine signaling, and down-modulation of surface expression of c-Mpl. This review will focus on these pathways in normal and neoplastic hematopoiesis.|*Hematopoiesis[MESH]|*Signal Transduction[MESH]|Humans[MESH]|Neoplasms[MESH]|Proto-Oncogene Mas[MESH]|Thrombopoietin/*metabolism[MESH] |
