+ |
Cullin 1-RBX1-Skp1 | down-regulates quantity by destabilization
polyubiquitination
|
NLRP3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272434 |
Lys689 |
GFLHNMPkEEEEEEK |
Homo sapiens |
A-549 Cell |
pmid |
sentence |
26037928 |
LPS exposure reduces the ubiquitin-mediated proteasomal processing of NALP3 by inducing levels of an E3 ligase component, FBXO3, which targets FBXL2. The latter is an endogenous mediator of NALP3 degradation. FBXL2 recognizes Trp-73 within NALP3 for interaction and targets Lys-689 within NALP3 for ubiquitin ligation and degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
FBXL2 | down-regulates quantity by destabilization
binding
|
NLRP3 |
0.358 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272432 |
Trp73 |
KAWAMAVwIFAAINR |
Homo sapiens |
A-549 Cell |
pmid |
sentence |
26037928 |
LPS exposure reduces the ubiquitin-mediated proteasomal processing of NALP3 by inducing levels of an E3 ligase component, FBXO3, which targets FBXL2. The latter is an endogenous mediator of NALP3 degradation. FBXL2 recognizes Trp-73 within NALP3 for interaction and targets Lys-689 within NALP3 for ubiquitin ligation and degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ROS | up-regulates activity
|
NLRP3 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256427 |
|
|
|
|
pmid |
sentence |
28531279 |
Different mechanisms have been proposed for NLRP3 activation, including potassium efflux, calcium influx, reactive oxygen species (ROS), oxidized mitochondrial DNA, translocation of cardiolipin from the inner mitochondrial membrane, phagosome destabilization, perturbation in cell volume and pore-formation mechanisms driven by the host or bacteria |
|
Publications: |
1 |
+ |
TLRs | up-regulates quantity by expression
|
NLRP3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256428 |
|
|
|
|
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 |
+ |
KCNJ8 | down-regulates activity
binding
|
NLRP3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262034 |
|
|
Homo sapiens |
|
pmid |
sentence |
31387986 |
We further show that Kir6.1 physically associates with NLRP3 and thus inhibits the interactions between the NLRP3 inflammasome subunits. Our results reveal a previously unrecognized function of Kir6.1 as a negative regulator of the NLRP3 inflammasome |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NLRP3 | form complex
binding
|
NLRP3 inflammasome |
0.739 |
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 |