3.4.15.1	amyloid beta-peptide(1-40) + H2O	cleavage at the Asp7-Ser9 bond. Compared with amyloid beta-peptide(1-40), aggregation and cytotoxic effects of the degradation products amyloid beta-peptide(1-7) and amyloid beta-peptide(8-40) are reduced ot virtually absent. The enzyme inhibits aggregation, deposition, and cytotoxicity of amyloid beta-peptide in vitro may affect susceptibility to Alzheimer‘s disease	
3.4.15.1	amyloid beta-protein 1-40 + H2O	ACE cleaves amyloid beta-protein 1-40 between Asp7 and Ser8	
3.4.15.1	amyloid beta-protein 1-42 + H2O	angiotensin-converting enzyme converts amyloid beta-protein 1-42 to amyloid beta-protein1-40. ACE regulates Abeta1-42/Abeta1-40 ratio in vivo by converting secreted Abeta1-42 to Abeta1-40 and degrading Abetas.The upregulation of ACE activity can be a novel therapeutic strategy for Alzheimer’s disease	
3.4.15.1	amyloid beta-protein 1-42 + H2O	angiotensin-converting enzyme converts amyloid beta-protein1-42 to amyloid beta-protein1-40. ACE regulates Abeta1-42/Abeta1-40 ratio in vivo by converting secreted Abeta1-42 to Abeta1-40 and degrading Abetas. The upregulation of ACE activity can be a novel therapeutic strategy for Alzheimer’s disease	
3.4.15.1	amyloid beta-protein 1-42 + H2O	ACE cleaves amyloid beta-protein 1-42 at multiple sites	
3.4.15.1	angiotensin I + H2O	-	
3.4.15.1	angiotensin I + H2O	enzyme plays a major role in blood pressure regulation	
3.4.15.1	angiotensin I + H2O	the enzyme plays an important role in blood pressure homeostasis	
3.4.15.1	angiotensin I + H2O	angiotensin II is a vasoconstrictor that raises blood pressure and is formed from angiotensin I by the angiotensin I converting enzyme in the reninangiotensin system	
3.4.15.1	angiotensin I + H2O	i.e. DRVYIHPFHL	
3.4.15.1	Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O	i.e. substance P, lung and brain ACE cleave substance P via two pathways. In one pathway ACE first releases Gly-Leu-Met-NH2 and then dipeptides sequentially from the carboxyl terminus. The other first produces Leu-Met-NH2 and then releases dipeptides to leave substance P(1-5)	
3.4.15.1	bradykinin + H2O	-	
3.4.15.1	bradykinin + H2O	degradation	
3.4.15.1	bradykinin + H2O	inactivation	
3.4.15.1	bradykinin + H2O	bradykinin is a nonapeptide released from high molecular weight kininogen, it exerts its vasodilatory effect mainly by stimulation of B2 receptors	
3.4.15.1	additional information	-	
3.4.15.1	additional information	potential role of follicular enzyme in early stages of follicular maturation and atresia	
3.4.15.1	additional information	the enzyme enhances presentation of certain endogenously synthesized peptides to major histocompatibility complex class-I-restricted cytotoxic T-lymphocytes	
3.4.15.1	additional information	primary enzyme that is involved in the degradation of Tyr-Gly-Gly-Phe-Met-Arg-Gly-Leu in brain	
3.4.15.1	additional information	may contribute to elevated blood pressure in hypertensive disease via conversion of angiotensin I to angiotensin II or inactivation of bradykinin	
3.4.15.1	additional information	the enzyme may play a role not only in the angiotensin-bradykinin system but also in the metabolism of circulating enkephalins and other bioactive peptides	
3.4.15.1	additional information	plays a role in blood pressure regulation	
3.4.15.1	additional information	angiotensin-converting enzyme-2 is a regulatory protein of the renin-angiotensin system. ACE2 interacts with calmodulin and this association down-regulates shedding of the ACE2 ectodomain	
3.4.15.1	additional information	neutral endopeptidase and angiotensin converting enzyme do not have additive effects regarding neuropeptide degradation	
3.4.15.1	additional information	somatic angiotensin I-converting enzyme plays a central role in blood pressure regulation	
3.4.15.1	additional information	ACE is a key regulator of blood pressure homeostasis	
3.4.15.1	additional information	ACE may influence trypsin biosynthesis in the larval gut by interacting with a trypsin-modulating oostatic factor	
3.4.15.1	additional information	ACE may play a role in human epidermis morphogenesis during fetal life and serve as an unrecognized marker for keratinocyte progenitor cells	
3.4.15.1	additional information	ACE degrades bradykinin, other vasoactive peptides, and activates angiotensin	
3.4.15.1	additional information	AnCE is a single domain protein with ACE activity, an ACE homologue	
3.4.15.1	additional information	complex formation witht e bradykinin B2 receptor	
3.4.15.1	additional information	ACE interacts with beta-arrestin1