Anti-Endothelin B Receptor/ET-B antibody

Supplementary info

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

Activity summary

Endothelin B receptor (ET-B) also known as endothelin receptor type B or EDNRB is a G protein-coupled receptor with a mass of approximately 50 kDa. It binds endothelin peptides which are 21-amino acid vasoconstrictor peptides critical in various physiological processes. ET-B is expressed in several tissues including vascular endothelial cells glial cells and various neurons within the central nervous system. This receptor plays a significant role in mediating the effects of the endothelin system by binding preferentially to endothelin-1 endothelin-2 and endothelin-3 with similar affinities.

Biological function summary

Endothelin B receptor is involved in the regulation of vascular tone blood pressure and fluid-electrolyte balance. It does not function in isolation; it often forms a complex with other proteins including G proteins which help transduce signals into cells leading to a variety of physiological responses. ET-B induces vasodilation by releasing nitric oxide and prostacyclin when activated on endothelial cells. It also plays a role in modulating neural crest cell migration during development which affects pigmentation and enteric nervous system formation.

Pathways

Endothelin B receptor is prominently involved in the endothelin signaling pathway and vascular endothelial growth factor (VEGF) pathway. In the endothelin pathway ET-B works alongside its relative endothelin A receptor (ET-A) to finely balance vasodilation and vasoconstriction processes. In the context of VEGF pathway ET-B is involved in angiogenesis aiding in the growth of new blood vessels. Its interactions include signaling molecules like nitric oxide synthase which contributes to its role in endothelial function and blood pressure regulation.

Associated diseases and disorders

Endothelin B receptor has substantial implications in conditions such as pulmonary arterial hypertension (PAH) and Hirschsprung's disease. In PAH dysregulation of endothelin system and overexpression of ET-B lead to abnormal vasoconstriction and vascular remodeling. The receptor's association with nitric oxide synthase highlights its influence in promoting pathological vascular changes in PAH. Additionally mutations in the EDNRB gene cause Hirschsprung's disease affecting neural crest cell migration and contributing to the failure of enteric nervous system development. ET-B's interactions and pathways highlight its importance in these medical conditions.