| + |
CASP6 | up-regulates activity 
cleavage
|
N |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260211 |
Asp400 |
VTLLPAAdMDDFSRQ |
Chlorocebus aethiops |
Vero Cell |
| pmid |
sentence |
| 18155731 |
Caspase-6 is activated through the intrinsic pathway and mediates C-terminal cleavage of SARS-CoV N at residues 400 and 403 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260212 |
Asp403 |
LPAADMDdFSRQLQN |
Chlorocebus aethiops |
Vero Cell |
| pmid |
sentence |
| 18155731 |
Caspase-6 is activated through the intrinsic pathway and mediates C-terminal cleavage of SARS-CoV N at residues 400 and 403 |
|
| Publications: |
2 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS |
| + |
UBE2I | up-regulates activity
sumoylation
|
N |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260263 |
Lys62 |
TALTQHGkEELRFPR |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 17037517 |
In this study, we identified Ubc9 as a host protein that interacts specifically with SARS-CoV N protein. This interaction was verified both in vivo and in vitro. Furthermore, we showed that, in addition to phosphorylation, the N protein was modified by covalent attachment of SUMO to its lysine 62 residue. Evidence provided demonstrated that sumoylation may promote homo-oligomerization of the protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
N | down-regulates activity 
|
IRF3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260337 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17108024 |
The data presented here indicate that N protein inhibits interferon production, while ORF 3b and ORF 6 proteins are able to inhibit both interferon production and interferon signaling. IRF-3 activation is inhibited in cells that express ORF 3b, ORF 6, or N protein, and NF-κB is inhibited in cells expressing N protein.ORF 3b, ORF 6, and N proteins all effectively inhibit phosphorylation of IRF-3.SARS-CoV ORF 3b, ORF 6, and N proteins all inhibit activation of IRF-3 by phosphorylation and binding of IRF-3 to a promoter with IRF-3 binding sites. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
N | down-regulates activity
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260340 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17108024 |
The data presented here indicate that N protein inhibits interferon production, while ORF 3b and ORF 6 proteins are able to inhibit both interferon production and interferon signaling. IRF-3 activation is inhibited in cells that express ORF 3b, ORF 6, or N protein, and NF-κB is inhibited in cells expressing N protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV CYTOKINE STORM, SARS-CoV FIBROSIS, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
N | down-regulates quantity 
binding
|
SMAD3/SMAD4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260427 |
|
|
Homo sapiens |
Lung |
| pmid |
sentence |
| 18055455 |
In this study, we demonstrate that SARS-associated coronavirus (SARS-CoV) nucleocapsid (N) protein potentiates transforming growth factor-beta (TGF-beta)-induced expression of plasminogen activator inhibitor-1 but attenuates Smad3/Smad4-mediated apoptosis of human peripheral lung epithelial HPL1 cells. The promoting effect of N protein on the transcriptional responses of TGF-beta is Smad3-specific. N protein associates with Smad3 and promotes Smad3-p300 complex formation while it interferes with the complex formation between Smad3 and Smad4. These findings provide evidence of a novel mechanism whereby N protein modulates TGF-beta signaling to block apoptosis of SARS-CoV-infected host cells and meanwhile promote tissue fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV FIBROSIS |
| + |
N | up-regulates activity 
|
JNK |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261131 |
|
|
Chlorocebus aethiops |
|
| pmid |
sentence |
| 15294014 |
Furthermore, N expression up-regulated the activity of stress-activated protein kinases, namely the JNK and p38 MAPK pathways. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
N | up-regulates activity
|
p38 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261132 |
|
|
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 15294014 |
Furthermore, N expression up-regulated the activity of stress-activated protein kinases, namely the JNK and p38 MAPK pathways. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION |
| + |
N | down-regulates quantity by repression
transcriptional regulation
|
Interferon-type-I |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260342 |
|
|
|
|
| pmid |
sentence |
| 17108024 |
The data presented here indicate that N protein inhibits interferon production, while ORF 3b and ORF 6 proteins are able to inhibit both interferon production and interferon signaling. |
|
| Publications: |
1 |
| Pathways: | COVID-19 Causal Network, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA |
| + |
N | up-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260204 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 15294014 |
In the present paper, we show that SARS-CoV N is capable of inducing apoptosis of COS-1 monkey kidney cells in the absence of growth factors by down-regulating ERK (extracellular-signal-regulated kinase), up-regulating JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) pathways, and affecting their downstream effectors. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260205 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 17453707 |
SARS-CoV Nucleocapsid Protein Induced Apoptosis of COS-1 Mediated by the Mitochondrial Pathway |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260199 |
|
|
Homo sapiens |
Lung Fibroblast Cell Line |
| pmid |
sentence |
| 16845612 |
Co-transfection of M and N enhances the induction of apoptosis by M or N alone, which also suggests that the structural proteins of SARS-CoV may play an important role not only in the process of invasion but also in the pathogenetic process in cells. |
|
| Publications: |
3 |
Organism: |
Chlorocebus Aethiops, Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV MAPK PERTURBATION, SARS-CoV FIBROSIS, SARS-CoV STRESS GRANULES |
| + |
N | up-regulates activity
|
AP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260725 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14623261 |
Taken together, we have shown that the coronavirus N protein can activate AP-1 signal transduction pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
FOS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260726 |
|
|
in vitro |
|
| pmid |
sentence |
| 14623261 |
The transcription factors c-Fos, FosB, CREB-1, and ATF2 were all activated by the addition of SARS-CoV N protein to the sample well |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260589 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18055455 |
In this study, we demonstrate that SARS-associated coronavirus (SARS-CoV) nucleocapsid (N) protein potentiates transforming growth factor-beta (TGF-beta)-induced expression of plasminogen activator inhibitor-1 but attenuates Smad3/Smad4-mediated apoptosis of human peripheral lung epithelial HPL1 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV FIBROSIS |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260727 |
|
|
in vitro |
|
| pmid |
sentence |
| 14623261 |
The transcription factors c-Fos, FosB, CREB-1, and ATF2 were all activated by the addition of SARS-CoV N protein to the sample well |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
CREB1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260729 |
|
|
in vitro |
|
| pmid |
sentence |
| 14623261 |
The transcription factors c-Fos, FosB, CREB-1, and ATF2 were all activated by the addition of SARS-CoV N protein to the sample well |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
FOSB |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260728 |
|
|
in vitro |
|
| pmid |
sentence |
| 14623261 |
The transcription factors c-Fos, FosB, CREB-1, and ATF2 were all activated by the addition of SARS-CoV N protein to the sample well |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
N | up-regulates activity
transcriptional regulation
|
PTGS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262314 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 16546436 |
SARS-CoV N protein activates COX-2 promoter and induces COX-2 protein expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV INFLAMMATORY RESPONSE |
| + |
N | up-regulates activity
binding
|
SMAD3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260434 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18055455 |
In this study, we demonstrate that SARS-associated coronavirus (SARS-CoV) nucleocapsid (N) protein potentiates transforming growth factor-beta (TGF-beta)-induced expression of plasminogen activator inhibitor-1 but attenuates Smad3/Smad4-mediated apoptosis of human peripheral lung epithelial HPL1 cells. The promoting effect of N protein on the transcriptional responses of TGF-beta is Smad3-specific. N protein associates with Smad3 and promotes Smad3-p300 complex formation while it interferes with the complex formation between Smad3 and Smad4. These findings provide evidence of a novel mechanism whereby N protein modulates TGF-beta signaling to block apoptosis of SARS-CoV-infected host cells and meanwhile promote tissue fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV FIBROSIS |
| + |
N | down-regulates activity
binding
|
EEF1A2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260260 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18448518 |
The nucleocapsid protein of severe acute respiratory syndrome coronavirus inhibits cell cytokinesis and proliferation by interacting with translation elongation factor 1alpha |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
N
- 
- 