EC Number   |
Expression |
Reference |
|---|
   3.4.17.23 | more |
renal ACE and ACE2 activities increase at 1 year in males, while there are no changes throughout development in females. Renal ACE and ACE2 mRNA and protein show no sex differences but increase by 1 year of age |
755365 |
| 3.4.17.23 | up |
angiotensin peptides modulate the expression of angiotensin converting enzyme II in the cardiovascular system, angiotensin II upregulates ACE2, modulated through activation of Ang II type 1 receptor, AT1R, and increases Ang-(1-7) formation from Ang II, and ACE2 expression is further enhanced by Ang-(1-7) in a positive feedback loop, molecular mechanism, overview. The upregulation is inhibited by Ang-(1-7) Mas receptor blockade through PD98059 |
710214 |
| 3.4.17.23 | up |
elevated expression in kidney and heart in a rat model with chronic heart failure |
731092 |
| 3.4.17.23 | up |
expression of ACE2 increases during aging in human lungs. ACE2 expression increases upon telomere shortening or dysfunction in cultured mammalian cells. This increase is controlled at the transcriptional level, and ACE2 promoter activity is DNA damage response-dependent |
764575 |
| 3.4.17.23 | up |
expression of ACE2 increases during aging in lungs. ACE2 expression increases upon telomere shortening or dysfunction. This increase is controlled at the transcriptional level, and ACE2 promoter activity is DNA damage response-dependent |
764575 |
| 3.4.17.23 | up |
high sucrose intake induces ACE2 expression in epididymal adipose tissue and kidney, leading to increased ACE2 and angiotensin-(1-7) levels in the adipose tissue |
710532 |
| 3.4.17.23 | up |
in lung tissues collected from mice that were sub-chronically exposed to air or 0.8 ppm ozone for three weeks, the ACE2 transcripts are significantly elevated in the parenchyma, but not in the extrapulmonary airways and alveolar macrophages. A significant proportion of additional known SARS-CoV-2 host susceptibility genes are upregulated in alveolar macrophages and parenchyma from ozone-exposed mice |
765794 |
| 3.4.17.23 | up |
infection with highly pathogenic avian influenza A H5N1 virus results in increased expression of angiotensin-converting enzyme 2 (ACE2) in serum |
732569 |
| 3.4.17.23 | up |
knockdown of TRIM28 induces enzyme (ACE2) expression. TRIM28 knockdown enhances interferon-gamma (IFN-gamma)-induced ACE2 expression through a mechanism involving upregulating IFN-gamma receptor 2 (IFNGR2) in both A549 and PAEpiCs. The upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells is partially reversed by dexamethasone in A-549 cells. TRIM28 is a novel regulator of ACE2 expression and SARS-CoV-2 cell entry |
762896 |
| 3.4.17.23 | up |
SARS-CoV-2 may bind and activate TLR4 to increase ACE2 expression, facilitating entry and causing hyperinflammation |
763421 |
