| + |
IFNAR | up-regulates quantity by expression 
transcriptional regulation
|
CCL2 |
0.325 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260851 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
IFNAR | up-regulates
|
Macrophage_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260848 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
3a | down-regulates quantity 
|
IFNAR |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260350 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20020050 |
The 3a protein was found to induce serine phosphorylation within the IFN alpha-receptor subunit 1 (IFNAR1) degradation motif and to increase IFNAR1 ubiquitination. Confocal microscopic analysis showed increased translocation of IFNAR1 into the lysosomal compartment and flow cytometry showed reduced levels of IFNAR1 in 3a-expressing cells. These results provide further mechanistic details of the pro-apoptotic effects of the SARS-CoV 3a protein, and suggest a potential role for it in attenuating interferon responses and innate immunity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
LMP2 | down-regulates quantity by destabilization
|
IFNAR |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266824 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19718044 |
The EBV-encoded Latent Membrane Proteins, LMP2A and LMP2B, Limit the Actions of Interferon by Targeting Interferon Receptors for Degradation.LMP2A and LMP2B increase the turnover and degradation of IFNAR1 and IFNGR1. LMP2A and LMP2B reduce the half-life of IFNAR1 and IFNGR1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection |
| + |
IFNAR | up-regulates quantity by expression
transcriptional regulation
|
CCL7 |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260852 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
IFNA1 | up-regulates activity 
binding
|
IFNAR |
0.631 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260334 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278538 |
Ifn-alpha, ifn-beta, and ifn-omega, induce somewhat different cellular effects but act through a common receptor complex, ifnar, composed of subunits ifnar-1 and ifnar-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
IFNAR | up-regulates activity
phosphorylation
|
PI3K |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260436 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21631354 |
These results indicate that NF-κB activation by IFN via the PI3K pathway is distinct from the ISRE-driven mechanism in regulating gene expression. Activation of PI3K/AKT by IFN has also been described through the insulin receptor substrate 1 (Uddin and others 1997) and through the direct interaction of PI3K with IFNAR1, which also leads to induction of NF-κB activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
Interferon-type-I | up-regulates activity
binding
|
IFNAR |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260331 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278538 |
Interferons have antiviral, antigrowth and immunomodulatory effects. The human type I interferons, IFN-alpha, IFN-beta, and IFN-omega, induce somewhat different cellular effects but act through a common receptor complex, IFNAR, composed of subunits IFNAR-1 and IFNAR-2. Human IFNAR-2 binds all type I IFNs but with lower affinity and different specificity than the IFNAR complex. Human IFNAR-1 has low intrinsic binding of human IFNs but strongly affects the affinity and differential ligand specificity of the IFNAR complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
IFNAR1 | form complex 
binding
|
IFNAR |
0.903 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260332 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278538 |
The human type I interferons, IFN-alpha, IFN-beta, and IFN-omega, induce somewhat different cellular effects but act through a common receptor complex, IFNAR, composed of subunits IFNAR-1 and IFNAR-2. Human IFNAR-2 binds all type I IFNs but with lower affinity and different specificity than the IFNAR complex. Human IFNAR-1 has low intrinsic binding of human IFNs but strongly affects the affinity and differential ligand specificity of the IFNAR complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNAR | up-regulates activity
binding
|
TYK2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260146 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15120645 |
Despite signaling through distinct receptor complexes, type I IFNs and IFN-lambda activate similar signaling events and biological activities, consistent with their common ability to mediate an antiviral state in cells (Fig. 6). In both cases, receptor engagement leads via the activation of the Jak kinases Jak1 and Tyk2 to the activation of the IFN-stimulated gene factor 3 (ISGF3) transcription complex, composed of latent transcriptional factors of the Signal Transducers and Activators of Transcription (STAT) family, Stat1 and Stat2, and of the interferon regulatory factor (IRF) IRF9 (ISGF3g or p48). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
IFNB1 | up-regulates activity
binding
|
IFNAR |
0.762 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260335 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278538 |
Ifn-alpha, ifn-beta, and ifn-omega, induce somewhat different cellular effects but act through a common receptor complex, ifnar, composed of subunits ifnar-1 and ifnar-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection, SARS-CoV CYTOKINE STORM |
| + |
IFNAR | up-regulates activity
binding
|
JAK1 |
0.728 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260147 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15120645 |
Despite signaling through distinct receptor complexes, type I IFNs and IFN-lambda activate similar signaling events and biological activities, consistent with their common ability to mediate an antiviral state in cells (Fig. 6). In both cases, receptor engagement leads via the activation of the Jak kinases Jak1 and Tyk2 to the activation of the IFN-stimulated gene factor 3 (ISGF3) transcription complex, composed of latent transcriptional factors of the Signal Transducers and Activators of Transcription (STAT) family, Stat1 and Stat2, and of the interferon regulatory factor (IRF) IRF9 (ISGF3g or p48). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
IFNW1 | up-regulates activity
binding
|
IFNAR |
0.731 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260336 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278538 |
Ifn-alpha, ifn-beta, and ifn-omega, induce somewhat different cellular effects but act through a common receptor complex, ifnar, composed of subunits ifnar-1 and ifnar-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNAR2 | form complex
binding
|
IFNAR |
0.903 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260333 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278538 |
The human type I interferons, IFN-alpha, IFN-beta, and IFN-omega, induce somewhat different cellular effects but act through a common receptor complex, IFNAR, composed of subunits IFNAR-1 and IFNAR-2. Human IFNAR-2 binds all type I IFNs but with lower affinity and different specificity than the IFNAR complex. Human IFNAR-1 has low intrinsic binding of human IFNs but strongly affects the affinity and differential ligand specificity of the IFNAR complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
IFNAR