| + |
NLRP3 inflammasome | up-regulates 
|
Pyroptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260356 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30166988 |
Once activated by a ligand, inflammasomes lead to the activation of a caspase. Activated caspases allow the release of mature forms of interleukin-1β and interleukin-18 and trigger a specific pro-inflammatory cell death termed pyroptosis. Accumulating data suggest that inflammasomes, mainly NLRP3, NLRP1, and AIM2, are involved in the generation of tissue damage and immune dysfunction after trauma. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Inflammosome Activation |
| + |
EIF2AK2 | up-regulates activity 
binding
|
NLRP3 inflammasome |
0.331 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263119 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 22801494 |
Here we identify a role for double-stranded RNA-dependent protein kinase (PKR, also known as EIF2AK2) in inflammasome activation. PKR physically interacts with several inflammasome components, including NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3), NLRP1, NLR family CARD domain-containing protein 4 (NLRC4), absent in melanoma 2 (AIM2), and broadly regulates inflammasome activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
3a | up-regulates activity
|
NLRP3 inflammasome |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260594 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 30761102 |
We found that the ion channel activity of SARS-CoV 3a protein is essential for activation of the NLRP3 inflammasome. In addition, both K+ efflux and mitochondrial ROS production are required for SARS-CoV 3a-mediated IL-1β secretion. In the case of SARS-CoV, the viroporin E forms forms Ca2+-permeable ion channels and activates the NLRP3 inflammasome.the 3a protein of SARS-CoV has the ability to induce the NLRP3 inflammasome activation by multiple mechanisms. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV INFLAMMATORY RESPONSE |
| + |
E | up-regulates activity
|
NLRP3 inflammasome |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261318 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32133002 |
Viroporins are small, highly hydrophobic proteins derived from viruses, which interact with membranes to modify the host cell's permeability to ions or other small molecules. Several viroporins are observed to localize to the Golgi apparatus and other cytoplasmic structures during viral infection.Examples include 2B proteins from EMCV, poliovirus, enterovirus 71 (EV71), and human rhinoviruses (HRV), the envelope (E) protein of severe acute respiratory syndrome coronavirus (SARS-CoV), as well as influenza virus M2 protein. These viroporins activate the NLRP3 inflammasome by inducing different ionic fluxes.N protein from SARS-CoV, cause the flux of calcium from intracellular storages to the cytosol, which is indispensable for NLRP3 activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
8b | up-regulates activity
binding
|
NLRP3 inflammasome |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260591 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 31231549 |
We found that ORF8b triggers robust NLRP3 inflammasome activation and IL-1β release. NLRP3 activation was accompanied by direct binding of ORF8b to the LRR domain of NLRP3. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV INFLAMMATORY RESPONSE |
| + |
CASP1 | form complex 
binding
|
NLRP3 inflammasome |
0.754 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256409 |
|
|
|
|
| pmid |
sentence |
| 30288079 |
Canonical inflammasomes form activation platforms for caspase-1. Their assembly depends on some dedicated cytosolic PRRs from the nucleotide-binding domain leucin-rich repeat (NLR) family including NLR and pyrin domain containing receptor 1 (NLRP1), NLRP3, and NLR and caspase recruitment domain containing receptor 4 (NLRC4); the AIM2-like receptors (ALR) family including absent in melanoma 2 (AIM2); or the tripartite motif (TRIM) family including pyrin. |
|
| Publications: |
1 |
| + |
NLRP3 | form complex
binding
|
NLRP3 inflammasome |
0.738 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256410 |
|
|
|
|
| pmid |
sentence |
| 30288079 |
Canonical inflammasomes form activation platforms for caspase-1. Their assembly depends on some dedicated cytosolic PRRs from the nucleotide-binding domain leucin-rich repeat (NLR) family including NLR and pyrin domain containing receptor 1 (NLRP1), NLRP3, and NLR and caspase recruitment domain containing receptor 4 (NLRC4); the AIM2-like receptors (ALR) family including absent in melanoma 2 (AIM2); or the tripartite motif (TRIM) family including pyrin. |
|
| Publications: |
1 |
| + |
NLRP3 inflammasome | up-regulates activity
cleavage
|
Caspase 1 complex |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256381 |
|
|
|
|
| pmid |
sentence |
| 30288079 |
Canonical inflammasomes form activation platforms for caspase-1. Their assembly depends on some dedicated cytosolic PRRs from the nucleotide-binding domain leucin-rich repeat (NLR) family including NLR and pyrin domain containing receptor 1 (NLRP1), NLRP3, and NLR and caspase recruitment domain containing receptor 4 (NLRC4); the AIM2-like receptors (ALR) family including absent in melanoma 2 (AIM2); or the tripartite motif (TRIM) family including pyrin. |
|
| Publications: |
1 |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
NLRP3 inflammasome |
0.361 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260328 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28531279 |
The activation of NLRP3 inflammasomes in macrophages requires two stimuli. The first signal, called priming, is provided by an inflammatory stimulus such as TLRs and TNF-α receptor (TNFR) that leads to NF-κB-mediated NLRP3 expression and post-translational modifications of NLRP3 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
PAMPs | up-regulates activity
|
NLRP3 inflammasome |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263127 |
|
|
|
|
| pmid |
sentence |
| 16037825 |
Among these sensors, members of the evolutionary conserved NLRs, together with AIM2 and pyrin, can assemble into a multimeric protein complex that is called the inflammasome (see poster).| An inflammasome assembles in response to a diverse range of pathogen-associated or danger-associated molecular patterns (PAMPs or DAMPs). The inflammasome platform leads to activation of caspase-1 through proximity-induced self-cleavage |
|
| Publications: |
1 |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
PYCARD | form complex
binding
|
NLRP3 inflammasome |
0.816 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256411 |
|
|
|
|
| pmid |
sentence |
| 30288079 |
Canonical inflammasomes form activation platforms for caspase-1. Their assembly depends on some dedicated cytosolic PRRs from the nucleotide-binding domain leucin-rich repeat (NLR) family including NLR and pyrin domain containing receptor 1 (NLRP1), NLRP3, and NLR and caspase recruitment domain containing receptor 4 (NLRC4); the AIM2-like receptors (ALR) family including absent in melanoma 2 (AIM2); or the tripartite motif (TRIM) family including pyrin. |
|
| Publications: |
1 |
| + |
NLRP3 inflammasome | up-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260346 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32133002 |
Both the NLRP3 inflammasome activation and the subsequent inflammation play significant roles in defending against viral infections. However, aberrant NLRP3 inflammasome activation or chronic inflammation can also lead to severe pathological injury. Accordingly, activation of the NLRP3 inflammasome and its associated inflammation is a double-edged sword for host to defense viral infection. Modulating the NLRP3 inflammasome activity can prove to be a promising strategy for the intervention of viral diseases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
3.0
NLRP3 inflammasome
CPX-4141