thrombopoietin
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A THPO gene provides instructions for making a protein called thrombopoietin that promotes the growth and division (proliferation) of cells. This protein attaches to (binds) and turns on (activates) the thrombopoietin receptor, which stimulates several signaling pathways that transmit chemical signals from outside the cell to the cell's nucleus. These pathways are important for controlling the production of blood cells.
Normal function
A THPO gene provides instructions for making a protein called thrombopoietin that promotes the growth and division (proliferation) of cells. This protein attaches to (binds) and turns on (activates) the thrombopoietin receptor, which stimulates several signaling pathways that transmit chemical signals from outside the cell to the cell's nucleus. These pathways are important for controlling the production of blood cells.
Thrombopoietin is especially important for the proliferation of certain blood cells called megakaryocytes, which produce platelets, the cells involved in blood clotting. Research suggests that thrombopoietin signaling may also play a role in the renewal of hematopoietic stem cells, which are stem cells located within the bone marrow that have the potential to develop into red blood cells, white blood cells, and platelets.
Conditions referring to this gene or chromosome
Other names
c-mpl ligand
megakaryocyte colony-stimulating factor
megakaryocyte growth and development factor
megakaryocyte stimulating factor
MGC163194
MGDF
MKCSF
ML
MPL ligand
MPLLG
myeloproliferative leukemia virus oncogene ligand
TPO
TPO_HUMAN
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Leitura adicional e referências
- thrombopoietin; MedlinePlus, National Library of Medicine.
- de Graaf CA, Metcalf D. Thrombopoietin and hematopoietic stem cells. Cell Cycle. 2011 May 15;10(10):1582-9. doi: 10.4161/cc.10.10.15619. Epub 2011 May 15.
- Ghilardi N, Skoda RC. A single-base deletion in the thrombopoietin (TPO) gene causes familial essential thrombocythemia through a mechanism of more efficient translation of TPO mRNA. Blood. 1999 Aug 15;94(4):1480-2. No abstract available.
- Ghilardi N, Wiestner A, Skoda RC. Thrombopoietin production is inhibited by a translational mechanism. Blood. 1998 Dec 1;92(11):4023-30.
- Majka M, Ratajczak J, Villaire G, Kubiczek K, Marquez LA, Janowska-Wieczorek A, Ratajczak MZ. Thrombopoietin, but not cytokines binding to gp130 protein-coupled receptors, activates MAPKp42/44, AKT, and STAT proteins in normal human CD34+ cells, megakaryocytes, and platelets. Exp Hematol. 2002 Jul;30(7):751-60. doi: 10.1016/s0301-472x(02)00810-x.
- Wiestner A, Schlemper RJ, van der Maas AP, Skoda RC. An activating splice donor mutation in the thrombopoietin gene causes hereditary thrombocythaemia. Nat Genet. 1998 Jan;18(1):49-52. doi: 10.1038/ng0198-49.
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