| + |
AGTR1 | up-regulates 
binding
|
GNAQ |
0.624 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106932 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11313903 |
These neuropeptide gpcrs are coupled to the activation of phospholipase c, and therefore to calcium ele- vation and protein kinase c (pkc) activation, through g proteins of the alfaq family. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates 
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260233 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Ang II binding to AT1 receptors has been implicated in inflammatory responses. Activation of this Ang II–AT1 receptor-dependent pathway is widely accepted to lead to organ damage and fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS |
| + |
MAS1 | down-regulates activity 
binding
|
AGTR1 |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260626 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 15809376 |
our findings demonstrate that the protein encoded by the Mas proto-oncogene exhibits direct antagonistic properties on the AT1 receptor in vitro and that this oligomeric interaction may represent a natural state for these receptors in vivo in some tissues. the present findings in native tissues suggest that the Mas receptor can act as an in vivo functional antagonist of the AT1 receptor owing to formation of a hetero-oligomeric complex |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS |
| + |
eprosartan | down-regulates activity
chemical inhibition
|
AGTR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258347 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1309870 |
The angiotensin II (AII) antagonist activity of (E)-alpha-[[2-butyl-1-[(4-carboxyphenyl)methyl]-1H-imidazol-5- yl]methylene]-2-thiophenepropanoic acid (SK&F 108566), was examined in a number of in vitro and in vivo assays. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates activity
binding
|
GNAI3 |
0.251 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256881 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
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 |
| + |
Ile(5)-angiotensin II | up-regulates activity
chemical activation
|
AGTR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257459 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates activity
binding
|
GNA15 |
0.472 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257223 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates
binding
|
GNA13 |
0.503 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-171760 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21289285 |
These results indicate that ang ii increases endothelial arginase activity/expression through galfa12/13 g proteins coupled to at(1) receptors and subsequent activation of rhoa/rock/p38 mapk pathways leading to endothelial dysfunction. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
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 |
| + |
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 |
| + |
AGTR1 | up-regulates
binding
|
GNG12 |
0.402 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-171763 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21289285 |
These results indicate that ang ii increases endothelial arginase activity/expression through galfa12/13 g proteins coupled to at(1) receptors and subsequent activation of rhoa/rock/p38 mapk pathways leading to endothelial dysfunction. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates activity
binding
|
GNAQ |
0.624 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257017 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates
|
Fibrosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260234 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32201502 |
Ang II binding to AT1 receptors has been implicated in inflammatory responses. Activation of this Ang II–AT1 receptor-dependent pathway is widely accepted to lead to organ damage and fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS |
| + |
AGTR1 | up-regulates quantity by expression
transcriptional regulation
|
PAX2 |
0.26 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252294 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15569307 |
Ang II up-regulated Pax-2 gene expression via AT2R in IRPTC (immortalized rat renal proximal tubular cells) |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Focal segmental glomerulosclerosis |
| + |
AGTR1 | down-regulates activity 
|
NPHS1 |
0.375 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253342 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 21982880 |
Ang II-receiving rats displayed diminished phosphorylation of nephrin but enhanced glomerular/podocyte injury and proteinuria when compared to control rats. These findings indicate that Ang II induces nephrin dephosphorylation and podocyte injury through a caveolin-1-dependent mechanism. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Focal segmental glomerulosclerosis |
| + |
valsartan | down-regulates activity
chemical inhibition
|
AGTR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258489 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8577935 |
The binding characteristics of the angiotensin AT1 receptor antagonist valsartan were investigated in different animal species and tissues. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates activity
binding
|
GNA14 |
0.463 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257133 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
telmisartan | down-regulates activity
chemical inhibition
|
AGTR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259072 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9878991 |
Telmisartan is a nonpeptide angiotensin II receptor antagonist which selectively and insurmountably inhibits the angiotensin II AT1 receptor subtype without affecting other receptor systems involved in cardiovascular regulation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AGTR1 | up-regulates activity
binding
|
GNAI1 |
0.251 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256738 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
AGTR1
- 
- 