| + |
ACE2 | up-regulates activity 
cleavage
|
Angiotensin-1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260221 |
His42 |
RVYIHPFhLVIHNES |
in vitro |
|
| pmid |
sentence |
| 11815627 |
The ACE2 hydrolytic activity is dependent on the C terminus sequence of the substrate, which is evident from the data with the angiotensin peptides. After 2 h, ACE2 hydrolyzes Ang I partially and Ang II completely, although there is no hydrolysis of angiotensin 1–9, angiotensin 1–7, and angiotensin 1–5, which possess the same N terminus. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260222 |
Pro40 |
GDRVYIHpFHLVIHN |
in vitro |
|
| pmid |
sentence |
| 11815627 |
The ACE2 hydrolytic activity is dependent on the C terminus sequence of the substrate, which is evident from the data with the angiotensin peptides. After 2 h, ACE2 hydrolyzes Ang I partially and Ang II completely, although there is no hydrolysis of angiotensin 1–9, angiotensin 1–7, and angiotensin 1–5, which possess the same N terminus. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
ACE2 | up-regulates activity
cleavage
|
AGT |
0.75 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256317 |
His42 |
RVYIHPFhLVIHNES |
in vitro |
|
| pmid |
sentence |
| 11815627 |
The ACE2 hydrolytic activity is dependent on the C terminus sequence of the substrate, which is evident from the data with the angiotensin peptides. After 2 h, ACE2 hydrolyzes Ang I partially and Ang II completely, although there is no hydrolysis of angiotensin 1–9, angiotensin 1–7, and angiotensin 1–5, which possess the same N terminus. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256315 |
Pro40 |
GDRVYIHpFHLVIHN |
in vitro |
|
| pmid |
sentence |
| 11815627 |
The ACE2 hydrolytic activity is dependent on the C terminus sequence of the substrate, which is evident from the data with the angiotensin peptides. After 2 h, ACE2 hydrolyzes Ang I partially and Ang II completely, although there is no hydrolysis of angiotensin 1–9, angiotensin 1–7, and angiotensin 1–5, which possess the same N terminus. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
PRTN3 | up-regulates activity
cleavage
|
AGT |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256314 |
Phe41 |
DRVYIHPfHLVIHNE |
in vitro |
|
| pmid |
sentence |
| 11747312 |
Cathepsin G, elastase, and proteinase 3 are serine proteinases released by activated neutrophils. Cathepsin G can cleave angiotensinogen to release angiotensin II, but this activity has not been previously reported for elastase or proteinase 3. In this study we show that elastase and proteinase 3 can release angiotensin I from angiotensinogen and release angiotensin II from angiotensin I and angiotensinogen. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
ELANE | up-regulates activity
cleavage
|
AGT |
0.279 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256313 |
Phe41 |
DRVYIHPfHLVIHNE |
in vitro |
|
| pmid |
sentence |
| 11747312 |
Cathepsin G, elastase, and proteinase 3 are serine proteinases released by activated neutrophils. Cathepsin G can cleave angiotensinogen to release angiotensin II, but this activity has not been previously reported for elastase or proteinase 3. In this study we show that elastase and proteinase 3 can release angiotensin I from angiotensinogen and release angiotensin II from angiotensin I and angiotensinogen. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
CTSG | up-regulates activity
cleavage
|
AGT |
0.627 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256312 |
Phe41 |
DRVYIHPfHLVIHNE |
in vitro |
|
| pmid |
sentence |
| 11747312 |
Cathepsin G, elastase, and proteinase 3 are serine proteinases released by activated neutrophils. Cathepsin G can cleave angiotensinogen to release angiotensin II, but this activity has not been previously reported for elastase or proteinase 3. In this study we show that elastase and proteinase 3 can release angiotensin I from angiotensinogen and release angiotensin II from angiotensin I and angiotensinogen. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
AGT | up-regulates activity
binding
|
REN |
0.927 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260224 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Renin is an aspartic protease that enzymatically cleaves its substrate angiotensinogen, which is produced by the liver, to form an inactive peptide: angiotensin (Ang)I or Ang (1–10). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Focal segmental glomerulosclerosis, SARS-CoV FIBROSIS |
| + |
SMOC1 | up-regulates quantity 
|
Angiotensin-2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260403 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 30127878 |
In conclusion, the results of the present study suggested that SMOC1 silencing suppressed the Ang II-induced myocardial fibrosis of mouse MFBs through affecting the BMP2/Smad signaling pathway. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ACE | up-regulates quantity
cleavage
|
Angiotensin-2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260236 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Ang I is subsequently converted into the major RAS effector peptide Ang II or Ang (1–8), through activity of the zinc-dependent protease ACE, which hydrolyzes two amino acids from the carboxy terminus of Ang I |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
AGT | up-regulates activity
binding
|
AGTR1 |
0.847 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252293 |
|
|
Rattus norvegicus |
Vascular Smooth Muscle Cell |
| pmid |
sentence |
| 17346243 |
AT(1) receptor (AngII type-1 receptor), a G-protein-coupled receptor, mediates most of the physiological and pathophysiological actions of AngII, and this receptor is predominantly expressed in cardiovascular cells, such as VSMCs (vascular smooth muscle cells) |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | COVID-19 Causal Network, Fibrosis, Focal segmental glomerulosclerosis, SARS-CoV FIBROSIS |
| + |
Angiotensin-2 | up-regulates activity
binding
|
AGTR2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260237 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Ang II initiates most of the RAS-attributed physiologic effects through selective interactions with G-proteincoupled Ang II type 1 (AT1) or type 2 (AT2) receptors and subsequent activation of distinct intra cellular signaling pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
AGT | up-regulates activity
|
TRPC6 |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253331 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24850910 |
We demonstrated that Ang II evokes concentration-dependent activation of podocyte TRPC6 channels |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Focal segmental glomerulosclerosis |
| + |
ACE2 | up-regulates quantity
cleavage
|
Angiotensin 1-7 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260227 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
At first, ACE2 has been demonstrated to induce conversion of Ang I into Ang (1–7) by means of intermediate production of Ang (1–9), a fragment with unknown function. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS |
| + |
Angiotensin 1-7 | down-regulates activity 
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260447 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24168260 |
We hypothesized that the ACE2/Ang-(1-7)/Mas axis protects against pulmonary fibrosis by inhibiting the MAPK/NF-κB pathway.In summary, our study demonstrate that exogenous Ang-(1-7) and ACE2 overexpression protect against BLM- or AngII-induced pulmonary fibrosis by down-regulating the MAPK/NF-κB pathway. However, constant infusion of Ang-(1-7) paradoxically initiates an inflammatory response in the lungs. The antifibrotic effects of Ang-(1-7) noted here make the heptapeptide a strong candidate for a therapeutic target in humans with pulmonary fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
ACE | up-regulates activity
cleavage
|
AGT |
0.775 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253326 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11076943 |
Angiotensin I-converting enzyme is a zinc metallopeptidase that plays an important role in blood pressure regulation by cleaving the inactive decapeptide angiotensin I to angiotensin II, a potent vasopressor octapeptide. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Focal segmental glomerulosclerosis, SARS-CoV FIBROSIS |
| + |
Angiotensin-1 | up-regulates activity
binding
|
ACE2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260226 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
At first, ACE2 has been demonstrated to induce conversion of Ang I into Ang (1–7) by means of intermediate production of Ang (1–9), a fragment with unknown function. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
REN | up-regulates activity
cleavage
|
AGT |
0.927 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252297 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16816138 |
Angiotensinogen, an _-glycoprotein, is released from the liver (152, 250, 444) and is cleaved in the circulation by the enzyme renin that is secreted from the juxtaglomerular apparatus of the kidney (245, 250, 540, 631) to form the decapeptide angiotensin (ANG) I |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Focal segmental glomerulosclerosis, SARS-CoV FIBROSIS |
| + |
REN | up-regulates quantity
cleavage
|
Angiotensin-1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260225 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Renin is an aspartic protease that enzymatically cleaves its substrate angiotensinogen, which is produced by the liver, to form an inactive peptide: angiotensin (Ang)I or Ang (1–10). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
AGT | up-regulates
binding
|
AGTR1 |
0.847 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145677 |
|
|
Homo sapiens |
Prostate Gland Cancer Cell |
| pmid |
sentence |
| 16597412 |
Endothelin-1 (et-1) and angiotensin ii (angii), two potent vasoactive peptides involved in the regulation of cardiovascular homeostasis, also induce mitogenic and pro-angiogenic responses in vitro and in vivo. Both peptides are produced by cleavage of inactive precursors by metalloproteases (endothelin-converting enzyme and angiotensin-converting enzyme, respectively) and activate two subtypes of membrane receptors (eta-r and etb-r for et-1, at1r and at2r for angii) that all belong to the superfamily of g-protein coupled receptors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Focal segmental glomerulosclerosis, SARS-CoV FIBROSIS |
| + |
Angiotensin-2 | up-regulates activity
binding
|
AGTR1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260238 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Ang II initiates most of the RAS-attributed physiologic effects through selective interactions with G-proteincoupled Ang II type 1 (AT1) or type 2 (AT2) receptors and subsequent activation of distinct intra cellular signaling pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
Angiotensin 1-7 | up-regulates activity
catalytic activity
|
Alamandine |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262307 |
|
|
in vitro |
|
| pmid |
sentence |
| 24389733 |
Newly discovered peptide, alamandine, have been identified. Alamandine is generated by catalysis of Ang A via ACE2 or directly from Ang-(1–7). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | SARS-CoV FIBROSIS |
| + |
Angiotensin 1-7 | up-regulates activity
binding
|
MAS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260229 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23488800 |
Recent advances have improved our understanding of the renin-angiotensin system (RAS). These have included the recognition that angiotensin (Ang)-(1-7) is a biologically active product of the RAS cascade. The identification of the ACE homologue ACE2, which forms Ang-(1-7) from Ang II, and the GPCR Mas as an Ang-(1-7) receptor have provided the necessary biochemical and molecular background and tools to study the biological significance of Ang-(1-7). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS |
| + |
AGT | up-regulates
|
AGTR2 |
0.819 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145680 |
|
|
Homo sapiens |
Prostate Gland Cancer Cell |
| pmid |
sentence |
| 16597412 |
Endothelin-1 (et-1) and angiotensin ii (angii), two potent vasoactive peptides involved in the regulation of cardiovascular homeostasis, also induce mitogenic and pro-angiogenic responses in vitro and in vivo. Both peptides are produced by cleavage of inactive precursors by metalloproteases (endothelin-converting enzyme and angiotensin-converting enzyme, respectively) and activate two subtypes of membrane receptors (eta-r and etb-r for et-1, at1r and at2r for angii) that all belong to the superfamily of g-protein coupled receptors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
Angiotensin-1 | up-regulates activity
binding
|
ACE |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260231 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Ang I is subsequently converted into the major RAS effector peptide Ang II or Ang (1–8), through activity of the zinc-dependent protease ACE, which hydrolyzes two amino acids from the carboxy terminus of Ang I |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
DPP3 | down-regulates quantity by destabilization 
cleavage
|
Angiotensin-2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268463 |
|
|
in vitro |
|
| pmid |
sentence |
| 34770898 |
Human dipeptidyl-peptidase III (hDPP III) is capable of specifically cleaving dipeptides from the N-terminal of small peptides with biological activity such as angiotensin II (Ang II, DRVYIHPF), and participates in blood pressure regulation, pain modulation, and the development of cancers in human biological activities. The binding of Ang II to hDPP III may lead to changes in the shape and size of subsite S1, an important catalytic site, so as to promote the decomposition of the substrate. |
|
| Publications: |
1 |
Organism: |
In Vitro |
3.0
AGT
- 
- 