| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261065 |
|
|
Homo sapiens |
Calu-3 Cell |
| pmid |
sentence |
| 27550352 |
Nafamostat also blocked MERS-CoV infection in vitro. This inhibition was most likely a result of inhibition of TMPRSS2 on the plasma membrane. Because MERS-CoV may infect cells via a TMPRSS2-independent endocytotic pathway, we evaluated the effects of nafamostat on MERS-CoV infection using an in vitro virus infection assay |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260736 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32142651 |
Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. The Cellular Serine Protease TMPRSS2 Primes SARS-2- S for Entry, and a Serine Protease Inhibitor Blocks SARS-CoV-2 Infection of Lung Cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263657 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25122198 |
we identified pro-hepatocyte growth factor (HGF) as a TMPRSS2 substrate and confirmed that HGF and it’s cognate receptor c-Met are activated in prostate cancers expressing TMPRSS2, a finding that also associated with the acquisition of a pro-invasive mesenchymal gene expression program. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Prostate Cancer |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260217 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32142651 |
Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261098 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32142651 |
Ndeed, the clinically proven serine protease inhibitor camostat mesylate, which is active against TMPRSS2 (Kawase et al., 2012), partially blocked SARS-2-S-driven entry into Caco-2 (Figure S3 B) and Vero-TMPRSS2 cells, efficiently blocked 2019-nCoV-S-driven entry into Caco-2 (TMPRSS2+) but not 293T (TMPRSS2- 110 ) cells while the CatB/L inhibitor E64d had the opposite effect |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253687 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21761340 |
The prostate-specific TMPRSS2 gene, while upregulated by AR activity in luminal cells, is also transcribed in basal populations, confirming that AR acts as an expression modulator. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253686 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20308527 |
We demonstrate that CHD8 directly associates with AR and that CHD8 and AR simultaneously localize to the TMPRSS2 enhancer after androgen treatment. In the LNCaP cell line, reduction of CHD8 levels by small interfering RNA treatment severely diminishes androgen-dependent activation of the TMPRSS2 gene. We demonstrate that the recruitment of AR to the TMPRSS2 promoter in response to androgen treatment requires CHD8 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251545 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24505269 |
Recurrent gene fusion between the androgen-regulated gene TMPRSS2 and members of the ETS transcription factor family, most commonly ERG, are present in about 50% of prostate cancer cases. Presence of this fusion gene is a critical event in the development of prostate cancer. the more aggressive phenotype that arises with the presence of TMPRSS2-ERG at least in part is caused by changes in the tumor stroma. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Prostate Cancer |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260284 |
|
|
Homo sapiens |
CACO-2 Cell |
| pmid |
sentence |
| 32142651 |
Indeed, the clinically proven serine protease inhibitor camostat mesylate, which is active against TMPRSS2 (Kawase et al., 2012), partially blocked SARS-2-S-driven entry into Caco-2 (Figure S3 B) and Vero-TMPRSS2 cells (Figure 4 A). Full inhibition was attained when camostat mesylate and E-64d, an inhibitor of CatB/L, were added (Figure 4A; Figure S3B), indicating that SARS-2-S can use both CatB/L as well as TMPRSS2 for priming in these cell lines. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY |
3.0
TMPRSS2
- 
- 
chemical inhibition
cleavage