By Kuter D.J., Li J.
The thrombopoietin receptor, c-mpl, is a member of the hematopoietin/cytokine receptor superfamily and contains duplicated hematopoietin receptor domain names (HRD). The proximal HRD is liable for receptor dimerization and consequent sign transduction and the distal HRD may well control its motion. The thrombopoietin receptor is located on many hematopoietic progenitors yet is essentially came upon on megakaryocytes and platelets. The platelet receptor is of excessive binding affinity (120-200pM) yet low floor density (30-60 websites in line with cell). Receptor binding via thrombopoietin ends up in the promoting of mobilephone growth/cellular differentiation, the prevention of apoptosis, and the internalization and degradation of the receptor-ligand advanced. lack of the distal HRD through fusion with the murine leukemia virus env protein ends up in unregulated expression of c-wpl and a myeloproliferative syndrome in mice. Mice poor within the thrombopoietin receptor produce 10-15% as many megakaryocytes and platelets as wild-type mice but additionally have 25-35% the traditional variety of erythroid and myeloid progenitors regardless of common peripheral purple and white blood mobile counts. No human abnormalities of c-mpl have not begun been defined and healing use of the soluble receptor has no longer but been verified.
