Anti-TPOR/MPL antibody [EPR24566-47] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The target TPOR/MPL also known as the MPL protein or Myeloproliferative Leukemia protein functions as a receptor for thrombopoietin (TPO). It is composed of 635 amino acids with a molecular weight of approximately 70 kDa. This protein is expressed primarily on the surface of hematopoietic progenitor cells megakaryocytes and platelets. The receptor a cell surface-bound protein plays a significant role by binding to TPO facilitating cellular signaling involved in cell proliferation and maturation.

Biological function summary

The TPOR/MPL protein promotes the growth and differentiation of multiple blood cell types through direct interactions with TPO. When TPO binds to MPL it triggers a signaling cascade essential for the regulation of platelet production and maintenance of hematopoiesis. This receptor forms part of a larger receptor complex that includes JAK2 protein kinase which further transduces signals for cell growth and survival. The engagement of JAK2 enhances the functional capability of MPL leading to the activation of various downstream effectors.

Pathways

The TPOR/MPL protein is central to the thrombopoietin signaling pathway facilitating the activation of downstream molecules like STAT3 and STAT5. These transcription factors activate gene expression critical for cell proliferation and survival. MPL is closely related to other hematopoietic receptors within the Jak-STAT pathway. The pathway is integral for hematopoietic stem cell function and involves interactions with proteins like EPO receptor which utilizes similar pathways for erythropoiesis.

Associated diseases and disorders

The TPOR/MPL protein is implicated in myeloproliferative disorders such as essential thrombocythemia and primary myelofibrosis. Mutations in the MPL gene can alter receptor function leading to uncontrolled cell proliferation. Such mutations often present in tandem with mutations in other proteins like JAK2 amplifying the disease processes. The inappropriate activation of the MPL signaling pathway results in excessive production of platelets or fibrosis within the bone marrow contributing significantly to disease phenotypes.