3.4.24.71	amyloid beta peptide + H2O	-	
3.4.24.71	amyloid-beta peptide + H2O	-	
3.4.24.71	amyloid-beta peptide + H2O	degradation	
3.4.24.71	angiotensin I + H2O	-	
3.4.24.71	angiotensin-I + H2O	degradation, no activity with angiotensin-II	
3.4.24.71	big endothelin + H2O	-	
3.4.24.71	big endothelin + H2O	activation	
3.4.24.71	big endothelin + H2O	ECE-1 is a membrane-bound metalloprotease responsible for production of vasoactive endothelin-1 from inactive big ET-1	
3.4.24.71	big endothelin + H2O	PKCepsilon regulates the expression of ECE-1 in the brain	
3.4.24.71	Big endothelin 1 + H2O	key enzyme in endothelin production, generates potent vasoconstrictor endothelin from its inactive precursor	
3.4.24.71	big endothelin-1 + H2O	key enzyme in the biosynthesis of the endothelins	
3.4.24.71	big endothelin-1 + H2O	ECE-1 is a critical enzyme in the production of the potent vasoconstrictor peptide endothelin, ET-1	
3.4.24.71	big endothelin-1 + H2O	-	
3.4.24.71	big endothelin-1 + H2O	final step of posttranslational processing of this peptide	
3.4.24.71	big endothelin-1 + H2O	most potent naturally occurring vasoconstrictor	
3.4.24.71	big endothelin-1 + H2O	activation	
3.4.24.71	big endothelin-1 + H2O	ECE-1 inhibition in MCF-7 breast cancer cells leads to a significantly decreased ET-1 expression and reduced cell invasiveness, overview	
3.4.24.71	big endothelin-1 + H2O	short-term endothelin-1 release is not involved in the isometric tension in response to different agonists, e.g. 15-E2t-IsoP, of human umbilical vein ring with or without endothelium, overview	
3.4.24.71	big endothelin-1 + H2O	big endothelin-1 is hydrolyzed at Asp18-Ile19	
3.4.24.71	big endothelin-3 + H2O	specific for this substrate, big-endothelin-1 is no substrate	
3.4.24.71	big endothelin-I + H2O	key enzyme in the biosynthesis of the endothelins	
3.4.24.71	bradykinin + H2O	-	
3.4.24.71	bradykinin + H2O	degradation	
3.4.24.71	calcitonin gene-related peptide + H2O	degradation, co-internalization with ECE-1 into early endosomes, calcitonin gene-related peptide degradation promotes CLR/RAMP1 recycling and beta-arrestin2 redistribution into the cytosol, ECE-1 inhibition or knockdown traps CLR/RAMP1 and beta-arrestin2 in endosomes and inhibits CLR/RAMP1 recycling and resensitization, whereas ECE-1 overexpression has the opposite effect, mechanism, overview	
3.4.24.71	additional information	endothelin-converting enzyme function as vasopeptidase	
3.4.24.71	additional information	isoforms of endothelin-converting enzyme-1, ECE-1a-d, are present in early endosomes, where they degrade neuropeptides and regulate post-endocytic sorting of receptors, ECE-1 does not regulate either the resensitization of receptors for peptides that are not ECE-1 substrates, e.g. angiotensin II, or the recycling of the bradykinin B2 receptor, which transiently interacts with beta-arrestins	
3.4.24.71	additional information	the enzyme catalyzes the final step in endothelin processing	
3.4.24.71	additional information	the enzyme is involved in chalizia, a granulomatous lesions of the eyelid	
3.4.24.71	additional information	the enzyme plays a crucial role in the regulation of vascular tone and endothelial function	
3.4.24.71	additional information	ECE-1 and endosomal acidification regulate the duration of substance P-induced ERK2 activation	
3.4.24.71	additional information	endothelin-converting enzyme-1 degrades substance P in early endosomes of epithelial cells and neurons to destabilize the endosomal mitogen-activated protein kinase signalosome and terminate signaling	
3.4.24.71	neurotensin + H2O	-	
3.4.24.71	preendothelin + H2O	-	
3.4.24.71	preproendothelin-1 + H2O	-	
3.4.24.71	proendothelin + H2O	-	
3.4.24.71	proendothelin-1 + H2O	activation	
3.4.24.71	somatostatin + H2O	-	
3.4.24.71	Substance P + H2O	-