EC Number   |
General Information |
Reference |
|---|
   3.4.17.23 | malfunction |
loss of ACE2 accelerates maladaptive left ventricular remodeling in response to myocardial infarction, MI, overview. ACE2 deficiency leads to increased matrix metalloproteinases 2 and 9 levels with MMP2 activation in the infarct and peri-infarct regions, as well as increased gelatinase activity leading to a disrupted extracellular matrix structure after MI. Loss of ACE2 also leads to increased neutrophilic infiltration in the infarct and peri-infarct regions, resulting in upregulation of inflammatory cytokines, interferon-gamma, interleukin-6, and the chemokine, monocyte chemoattractant protein-1, as well as increased phosphorylation of ERK1/2 and JNK1/2 signaling pathways |
708141 |
| 3.4.17.23 | malfunction |
loss of ACE2 function is implicated in severe acute respiratory syndrome, SARS, pathogenesis |
707074 |
| 3.4.17.23 | malfunction |
mice infected with influenza H7N9 virus downregulate ACE2 protein markedly on day 3 after infection |
732911 |
| 3.4.17.23 | malfunction |
postural tachycardia syndrome is associated with increased plasma angiotensin-II. ACE2 effects are blunted in low flow postural tachycardia syndrome, POTS, and restored by the ACE2 product angiotensin-(1-7) |
708685 |
| 3.4.17.23 | metabolism |
ACE2 ia a component of the renin-angiotensin system, RAS |
710171 |
| 3.4.17.23 | metabolism |
induced dysregulation of the enzyme (ACE2) by SARS-CoV-2 plays a key role in COVID-19 severity. Downregulation of ACE2 can be one of the main causes of SARS-CoV-2 symptoms. COVID-19 severity can be changed by reduction in ACE2 products such as Ang (1-7), Ang (1-9), apelin (1-12) and accumulation of substrates such as apelin (1-13) and Ang II. The downregulation of ACE2, accumulated apelin (1-13) can stimulate the pulmonary embolism |
762787 |
| 3.4.17.23 | metabolism |
the enzyme is involved in the renin-angiotensin system (RAS), which includes angiotensin I, angiotensin (Ang)II, and peptides angiotensin-(1-9) and angiotensin-(1-7) derived by C-terminal cleavage of their particular antecessors by angiotensin converting enzyme (ACE)1 or ACE2, overview |
753311 |
| 3.4.17.23 | physiological function |
ACE 2 balances the status of the renin-angiotensin system by degrading angiotensin II and generating angiotensin-(1-7). ACE2 induces overexpression of connective tissue growth factor, which is inhibited by blockade of theMas receptor with A779, overview |
708195 |
| 3.4.17.23 | physiological function |
ACE2 binds the prototype SARS-CoV-2 receptor-binding domain with a dissociation constant (KD) of 24.63 nM. Receptor-binding domains from SARS-CoV-2 variants alpha, beta, and gamma demonstrate enhanced affinities, ranging from 1.78- to 4.56fold increase. Variant omicron, along with delta receptor-binding domain, shows no significant change in binding affinities when compared with those of the prototype domain |
764429 |
| 3.4.17.23 | physiological function |
ACE2 functions as a carboxypeptidase that can cleave several endogenous substrates, including angiotensin II, thus regulating blood pressure and vascular tone |
763217 |
