Gene Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 Biomarker disease BEFREE After IMD<sub>1-53</sub> treatment, inflammation caused by sepsis in vivo was greatly reduced, as shown by the downregulation of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), nucleotide-binding domain and leucine-rich repeat containing family, pyrin containing 3 (NLRP3), pro-IL-1β, caspase 1, and nuclear translocation of nuclear factor-κB (NF-kB) protein levels. 29192367 2018
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 Biomarker disease BEFREE NLRP3 inflammasome and RhoA contribute to sepsis and intestinal inflammation. 31835087 2020
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 Biomarker disease BEFREE Moreover, we report that ABRO1 deficiency results in a remarkable attenuation in the syndrome severity of NLRP3-associated inflammatory diseases, including MSU- and Alum-induced peritonitis and LPS-induced sepsis in mice. 30787184 2019
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 AlteredExpression disease BEFREE <b>Conclusion:</b> Pulegone exerts anti-inflammatory effects on LPS-induced sepsis mice via inhibition of the NLRP3 expression. 31134844 2019
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 Biomarker disease BEFREE An inducer and inhibitor of autophagy and the NLRP3 inflammasome were administered to investigate the detailed mechanism of action of H2 treatment in sepsis. 31432098 2019
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 Biomarker disease BEFREE In human THP-1 cells, anti-IL-31/anti-IL-31 receptor (R) neutralizing antibody enhanced NLRP3 expression as well as IL-1β activation, suggesting a role of the IL-31-IL-31R-NLRP3-IL-1β signaling axis in the physiological status of sepsis. 29896237 2018
Entrez Id: 114548
Gene Symbol: NLRP3
NLRP3
0.100 Biomarker disease BEFREE These findings enhance our understanding of the critical role of NLRP3 in modulating autophagy and phagocytosis in neutrophils and suggest that therapies should be targeted to modulate autophagy and phagocytosis in neutrophils to control bacterial burden in tissues during CLP-induced polymicrobial sepsis. 28031338 2017