Autophagosome-lysosome mediated secretion of the thrombopoietin receptor is modulated by distinct driver mutations of myeloproliferative neoplasm.

The maintenance of the haematopoietic stem cells and the production of platelets thereof is acutely dependent upon the thrombopoietin receptor (TpoR). TpoR dimerizes in the presence of its ligand thrombopoietin leading to the activation of downstream JAK2-STAT signalling. Alternatively, the receptor dimerizes in the presence of activating mutations of JAK2 (JAK2 V617F), calreticulin or TpoR leading to myeloproliferation.