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Appears in Networks 4

In-Edges 19

a(CHEBI:"amyloid-beta") increases act(p(HGNC:NLRP3)) View Subject | View Object

A few molecules, such as amyloid-β, can induce both NLRP3 priming through TLR activation and NLRP3 inflammasome activation68. PubMed:23702978

Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

tloc(a(CHEBI:"calcium(2+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) increases act(p(HGNC:NLRP3)) View Subject | View Object

This channel senses intracellular ROS and responds by opening itself to facilitate Ca2+ influx into the cell; this is intriguing considering that both ion fluxes and the oxidative state (see below) have important roles in NLRP3 inflammasome activation. PubMed:23702978

composite(p(FPLX:HSP90), p(HGNC:SUGT1)) increases act(p(HGNC:NLRP3)) View Subject | View Object

Finally, heat shock proteins (HSPs) also have important roles in the regulation of cell death, and it has been shown that HSP90 and the cochaperone ubiquitin ligase-associated protein SGT1 are required for NLRP3 activation (REF. 129). PubMed:23702978

m(HGNC:MIR223) decreases p(HGNC:NLRP3) View Subject | View Object

Furthermore, the amount of NLRP3 mRNA is tightly regulated by the microRNA miR-223, which leads to decreased NLRP3 protein levels and, thus, influences the threshold of NLRP3 activation74,75. PubMed:23702978

Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

act(p(FPLX:TLR)) increases p(HGNC:NLRP3) View Subject | View Object

First, a bacterial Toll-like receptor (TLR) activator leads to cellular priming and upregulation of NLRP3 and pro-IL-1β expression (the priming checkpoint in the standard model)37,38. PubMed:23702978

p(FPLX:TNFRSF) increases p(HGNC:NLRP3) View Subject | View Object

Many innate immune signalling or cytokine receptors, such as the TNFR, activate transcription of NLRP3 and thereby influence the susceptibility of immune cells to NLRP3 inflammasome triggers37,38 (FIG. 2). PubMed:23702978

p(HGNC:IFNG) decreases act(p(HGNC:NLRP3)) View Subject | View Object

In addition, T cell-derived IFNγ has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity. PubMed:23702978

p(HGNC:NLRP3, pmod(NO)) decreases act(p(HGNC:NLRP3)) View Subject | View Object

In addition, T cell-derived IFNγ has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity. PubMed:23702978

p(HGNC:TRPM2) increases act(p(HGNC:NLRP3)) View Subject | View Object

Another transient receptor potential channel — TRPM2 — has also been implicated in NLRP3 activation in response to crystalline substances88. PubMed:23702978

a(CHEBI:"amyloid-beta") association p(HGNC:NLRP3) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

a(MESH:Astrocytes) increases p(HGNC:NLRP3) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

a(MESH:Microglia) increases p(HGNC:NLRP3) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

a(CHEBI:heme) increases p(HGNC:NLRP3) View Subject | View Object

Most studies concerning the pathophysiological roles of heme have focused on the protective effect of the heme-degrading enzyme, heme oxygenase 1 (HO-1) [25] (Box 2), and on the effect of this danger-associated molecule on cells, leading to oxidative stress, TLR4 signaling [26,27], and NLRP3 inflammasome activation [28] (Box 4). PubMed:26875449

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Text Location
Review

a(CHEBI:heme) positiveCorrelation p(HGNC:NLRP3) View Subject | View Object

It has been reported that an increase in extracellular heme activates NLRP3 expression, triggering inflammasome activation [28]. PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

p(HGNC:CASP1) positiveCorrelation p(HGNC:NLRP3) View Subject | View Object

As a component of inflammasome, NLRP3 is the best characterized member of NLRs, which recruits and activates caspase-1 via the adapter molecule ASC (apoptosis- associated speck-like protein containing caspase activation and recruitment domain) [8, 9]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

path(MESH:"Brain Edema") positiveCorrelation p(HGNC:NLRP3) View Subject | View Object

. Interestingly, NLRP3 knockdown and mROS inhibitors reduce brain edema and improve neurological functions (Ma et al., 2014). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

Out-Edges 9

p(HGNC:NLRP3) association a(CHEBI:"amyloid-beta") View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

act(p(HGNC:NLRP3)) increases sec(p(HGNC:CASP1)) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

p(HGNC:NLRP3) positiveCorrelation p(HGNC:CASP1) View Subject | View Object

As a component of inflammasome, NLRP3 is the best characterized member of NLRs, which recruits and activates caspase-1 via the adapter molecule ASC (apoptosis- associated speck-like protein containing caspase activation and recruitment domain) [8, 9]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

p(HGNC:NLRP3) positiveCorrelation path(MESH:"Brain Edema") View Subject | View Object

. Interestingly, NLRP3 knockdown and mROS inhibitors reduce brain edema and improve neurological functions (Ma et al., 2014). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

p(HGNC:NLRP3) increases path(MESH:Atherosclerosis) View Subject | View Object

Indeed, TLRs and NLRP3 have been associated with atherosclerosis development. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

p(HGNC:NLRP3) positiveCorrelation a(CHEBI:heme) View Subject | View Object

It has been reported that an increase in extracellular heme activates NLRP3 expression, triggering inflammasome activation [28]. PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

p(HGNC:NLRP3) increases act(a(MESH:Inflammasomes)) View Subject | View Object

It has been reported that an increase in extracellular heme activates NLRP3 expression, triggering inflammasome activation [28]. PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.