| 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 |
| + |
FURIN | up-regulates activity 
cleavage
|
S |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262305 |
|
|
Homo sapiens |
Calu-3 Cell |
| pmid |
sentence |
| 32362314 |
Here, we report that the cellular protease furin cleaves the spike protein at the S1/S2 site and that cleavage is essential for S-protein-mediated cell-cell fusion and entry into human lung cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262303 |
|
|
Homo sapiens |
Calu-3 Cell |
| pmid |
sentence |
| 32362314 |
Here, we report that the cellular protease furin cleaves the spike protein at the S1/S2 site and that cleavage is essential for S-protein-mediated cell-cell fusion and entry into human lung cells. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV ATTACHMENT AND ENTRY |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262304 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32404436 |
TMPRSS2 and TMPRSS4 serine proteases mediate this process by inducing cleavage of the S protein and enhancing membrane fusion. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262306 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32404436 |
TMPRSS2 and TMPRSS4 serine proteases mediate this process by inducing cleavage of the S protein and enhancing membrane fusion. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV ATTACHMENT AND ENTRY |
| + |
CTSL | up-regulates activity
cleavage
|
S |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260737 |
|
|
Homo sapiens |
CACO-2 Cell |
| pmid |
sentence |
| 32142651 |
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 |
| + |
CTSB | up-regulates activity
cleavage
|
S |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260738 |
|
|
Homo sapiens |
CACO-2 Cell |
| pmid |
sentence |
| 32142651 |
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 |
| + |
S | down-regulates activity 
binding
|
ACE2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260742 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32125455 |
SARS-CoV and likely SARS-CoV-2 lead to downregulation of the ACE2 receptor, but not ACE, through binding of the spike protein with ACE2. This leads to viral entry and replication, as well as severe lung injury. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS |
| + |
S | form complex 
binding
|
CoV2 Spike protein-ACE2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260739 |
|
|
Chlorocebus aethiops |
Vero Cell |
| pmid |
sentence |
| 32155444 |
We report here that ACE2 could mediate SARS-CoV-2 S-mediated entry into cells, establishing it as a functional receptor for this newly emerged coronavirus. The SARS-CoV-2 SB engages human ACE2 (hACE2) with comparable affinity to SARS-CoV SB from viral isolates associated with the 2002–2003 epidemic (i.e., binding with high affinity to hACE2). Tight binding to hACE2 could partially explain the efficient transmission of SARS-CoV-2 in humans, as was the case for SARS-CoV. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY |
| + |
S | form complex
binding
|
CoV2 spike protein-NRP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261671 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| other |
Neuropilin-1 facilitates SARS-CoV-2 cell entry and provides a possible pathway into the central nervous system To determine whether SARS-CoV-2 uses NRP1 for virus entry, we generated replication deficient lentiviruses pseudotyped with SARS-CoV-2 spike protein (S) that drive expression of green fluorescent protein (GFP) upon infection. When expressed alone, ACE2 rendered cells susceptible to infection (Fig. 1a). NRP1 alone allowed lower, yet detectable levels of infection, both in HEK-293T and in Caco2 cells (Fig. 1a,b), while cells transfected with plasmids encoding only TMPRSS2 were not infected (Fig. 1a). The co-expression of TMPRSS2 with either ACE2 or NRP1 potentiated the infection, with ACE2 together with TMPRSS2 being twice as efficient as NRP1 with TMPRSS2 (Fig. 1c) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV ATTACHMENT AND ENTRY |
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