EC Number   |
Natural Substrates |
|---|
   3.4.17.23 | angiotensin II + H2O |
angiotensin II has many adverse cardiovascular effects when acting through the AT1 receptor |
| 3.4.17.23 | angiotensin II + H2O |
high levels of angiotensin II induces pulmonary arterial hypertension |
| 3.4.17.23 | more |
ACE2 is a crucial SARS-CoV receptor. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway |
| 3.4.17.23 | more |
angiotensin-converting enzyme 2: a functional receptor for SARS coronavirus |
| 3.4.17.23 | more |
presence of ACE2 alone is not sufficient for maintaining viral infection. Other virus receptors or coreceptors may be required in different tissues |
| 3.4.17.23 | more |
the enzyme has a function in blood pressure regulation, blood flow and fluid regulation. Loss of ACE2 impairs heart function |
| 3.4.17.23 | more |
the enzyme is involved in diesease condition including hypertension, diabetes and cardiac function. ACE2 is the SARS virus receptor |
| 3.4.17.23 | more |
ACE2 ectodomain shedding and/or sheddase(s) activation regulated by calmodulin is independent from the phorbol ester-induced shedding |
| 3.4.17.23 | more |
ACE2 is down-regulated and ACE is up-regulated in hypertensive nephropathy. Ang II, once released, can act to up-regulate ACE but down-regulate ACE2 via the AT1 receptor-mediated mechanism. Activation of the ERK1/2 and p38 MAP kinase pathway may represent a key mechanism by which Ang II down-regulates ACE2 |
| 3.4.17.23 | more |
ACE2 is involved in the regulation of heart function, ACE 2 is a functional receptor for the coronavirus that causes the severe acute respiratory syndrome |
