Description
Recombinant Human ECE1 Protein (His Tag) | PKSH033691 | Gentaur US, UK & Europe Disrtribition
Synonyms: Endothelin-converting enzyme 1; ECE-1
Active Protein: N/A
Activity: Recombinant Human Endothelin-converting Enzyme 1 is produced by our Mammalian expression system and the target gene encoding Gln90-Trp770 is expressed with a 8His tag at the N-terminus.
Protein Construction: Recombinant Human Endothelin-converting Enzyme 1 is produced by our Mammalian expression system and the target gene encoding Gln90-Trp770 is expressed with a 8His tag at the N-terminus.
Fusion Tag: N-His
Species: Human
Expressed Host: Human Cells
Shipping: This product is provided as lyophilized powder which is shipped with ice packs.
Purity: > 95 % as determined by reducing SDS-PAGE.
Endotoxin: < 1.0 EU per μg as determined by the LAL method.
Stability and Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Molecular Mass: 78.8 kDa
Formulation: Lyophilized from a 0.2 μm filtered solution of PBS, pH7.4.
Reconstitution: Please refer to the printed manual for detailed information.
Background: Endothelin-Converting Enzyme-1 (ECE-1) is a single-pass type I I transmembrane (TM) protein with a short cytoplasmic tail and a large ectodomain. ECE-1 is a zinc protease of the neprilysin (NEP) family, which also includes ECE-2, PEX, XCE, DINE, and Kell, and several NEP-like proteins. It is widely expressed and has several alternatively spliced forms that differ in their TM domain or cytoplasmic tail. All isoforms of ECE-1 are expressed in umbilical vein endothelial cells, polynuclear neutrophils, fibroblasts, atrium cardiomyocytes and ventricles. Endothelin-converting enzyme-1 is involved in the proteolytic processing of Endothelin-1 (EDN1), Endothelin-2 (EDN2), and Endothelin-3 (EDN3) to biologically active peptides. Defects in ECE1 are a cause of Hirschsprung disease, cardiac defects and autonomic dysfunction (HSCRCDAD). It is a form of Hirschsprung disease with skip-lesions defects, craniofacial abnormalities and other dysmorphic features, and autonomic dysfunction.
Research Area: Signal Transduction, Cardiovascular, Cancer, metabolism,
