1. Catalog
  2. Nodes
  3. p(MGI:Nlrp3)

p(MGI:Nlrp3)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
Nlrp3
Namespace
MGI
Namespace Version
20170725
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/mgi-mouse-genes/mgi-mouse-genes-20170725.belns

Appears in Networks 2

The role of inflammasome in Alzheimer’s disease v1.0.3

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 8

a(CHEBI:heme) positiveCorrelation act(p(MGI:Nlrp3)) View Subject | View Object

These results demonstrate that free heme induces IL-1b through activating NLRP3 inflammasome via ASC and suggest that free heme plays an essential role in inflammation response as a dangerous signal. PubMed:24464629

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

p(MGI:Hmox1) negativeCorrelation p(MGI:Nlrp3) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Il1b) positiveCorrelation act(p(MGI:Nlrp3)) View Subject | View Object

As expected, NLRP3+/+ macrophages were efficiently stimulated to secrete IL-1b by heme, and displayed dose-dependent (up to 40 lM) manner. PubMed:24464629

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

p(MGI:Il1b) positiveCorrelation act(p(MGI:Nlrp3)) View Subject | View Object

These results demonstrate that free heme induces IL-1b through activating NLRP3 inflammasome via ASC and suggest that free heme plays an essential role in inflammation response as a dangerous signal. PubMed:24464629

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

p(MGI:P2rx4) positiveCorrelation act(p(MGI:Nlrp3)) View Subject | View Object

These results strongly suggest that heme activates NLRP3 through P2X receptors, especially P2X4R and P2X7R. PubMed:24464629

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

p(MGI:P2rx7) positiveCorrelation act(p(MGI:Nlrp3)) View Subject | View Object

Furthermore, P2X7R was reported that participates in NLRP3 activation in renal inflammation and injury induced by high-fat diet [29]. PubMed:24464629

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

p(MGI:P2rx7) positiveCorrelation act(p(MGI:Nlrp3)) View Subject | View Object

These results strongly suggest that heme activates NLRP3 through P2X receptors, especially P2X4R and P2X7R. PubMed:24464629

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

path(MESH:Inflammation) positiveCorrelation p(MGI:Nlrp3) View Subject | View Object

These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629

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

Out-Edges 12

p(MGI:Nlrp3) increases p(MGI:Il1b) View Subject | View Object

A recent report shows that IL-18 and IL-1β are secreted from primed murine dendritic cells in response to Listeria protein p60, but inhibiting NLRP3 reduces the production of IL-1β, but not IL-18 secretion (Schmidt and Lenz, 2012) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Dendritic Cells
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(MGI:Nlrp3) increases bp(GO:"amyloid-beta formation") View Subject | View Object

In support, knockout of NLRP3 and caspase-1 have been shown to suppress amyloidogenesis and neuropathology, and improve cognition in AD transgenic mice (Heneka et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph

p(MGI:Nlrp3) increases a(MESH:Neuropathology) View Subject | View Object

In support, knockout of NLRP3 and caspase-1 have been shown to suppress amyloidogenesis and neuropathology, and improve cognition in AD transgenic mice (Heneka et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph

p(MGI:Nlrp3) decreases bp(GO:cognition) View Subject | View Object

In support, knockout of NLRP3 and caspase-1 have been shown to suppress amyloidogenesis and neuropathology, and improve cognition in AD transgenic mice (Heneka et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph

act(p(MGI:Nlrp3)) positiveCorrelation p(MGI:Il1b) View Subject | View Object

As expected, NLRP3+/+ macrophages were efficiently stimulated to secrete IL-1b by heme, and displayed dose-dependent (up to 40 lM) manner. PubMed:24464629

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

act(p(MGI:Nlrp3)) positiveCorrelation p(MGI:Il1b) View Subject | View Object

These results demonstrate that free heme induces IL-1b through activating NLRP3 inflammasome via ASC and suggest that free heme plays an essential role in inflammation response as a dangerous signal. PubMed:24464629

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

act(p(MGI:Nlrp3)) positiveCorrelation a(CHEBI:heme) View Subject | View Object

These results demonstrate that free heme induces IL-1b through activating NLRP3 inflammasome via ASC and suggest that free heme plays an essential role in inflammation response as a dangerous signal. PubMed:24464629

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

act(p(MGI:Nlrp3)) positiveCorrelation p(MGI:P2rx7) View Subject | View Object

Furthermore, P2X7R was reported that participates in NLRP3 activation in renal inflammation and injury induced by high-fat diet [29]. PubMed:24464629

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

act(p(MGI:Nlrp3)) positiveCorrelation p(MGI:P2rx7) View Subject | View Object

These results strongly suggest that heme activates NLRP3 through P2X receptors, especially P2X4R and P2X7R. PubMed:24464629

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

act(p(MGI:Nlrp3)) positiveCorrelation p(MGI:P2rx4) View Subject | View Object

These results strongly suggest that heme activates NLRP3 through P2X receptors, especially P2X4R and P2X7R. PubMed:24464629

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

p(MGI:Nlrp3) positiveCorrelation path(MESH:Inflammation) View Subject | View Object

These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629

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

p(MGI:Nlrp3) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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.