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Entity

Name
P2rx4
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

In-Edges 3

a(CHEBI:heme) 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:Il1b) positiveCorrelation p(MGI:P2rx4) View Subject | View Object

Therefore, knockdown of P2X4R and double knockdown of P2X7R plus P2X4R were performed by shRNA in macrophages and the result showed that P2X4R knockdown also partially inhibit the heme induced IL-1b secretion and double knockdown of P2X7R plus P2X4R almost completely depressed the IL-1b secretion (Fig. 3d). 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

Out-Edges 7

p(MGI:P2rx4) increases act(complex(GO:"NLRP1 inflammasome complex")) View Subject | View Object

Given that P2X4 and P2X7 are the major purinergic P2X receptor subtypes, a study of spinal cord injury in P2X4 knock-out mice showed a significant reduction in inflammasome activation and proinflammatory cytokine production as compared to wild type (de Rivero Vaccari et al., 2012), supporting the involvement of purinergic receptor P2X4 in the activation of the NLRP1 inflammasome PubMed:24561250

Annotations
Confidence
High

p(MGI:P2rx4) increases p(HGNC:IL1B) View Subject | View Object

However, upon further study of purinergic receptor P2X4 knockout mice with spinal cord injury, the production of IL-1β but not of IL-18 reduces in the neurons as compared with wild-type mice (de Rivero Vaccari et al., 2012) PubMed:24561250

p(MGI:P2rx4) increases p(HGNC:IL1B) View Subject | View Object

P2X4 knock-out mice has been shown to decrease the level of IL-1β and to have impair inflammasome signaling (de Rivero Vaccari et al., 2012) PubMed:24561250

p(MGI:P2rx4) increases act(complex(GO:"inflammasome complex")) View Subject | View Object

P2X4 knock-out mice has been shown to decrease the level of IL-1β and to have impair inflammasome signaling (de Rivero Vaccari et al., 2012) PubMed:24561250

p(MGI:P2rx4) positiveCorrelation p(MGI:Il1b) View Subject | View Object

Therefore, knockdown of P2X4R and double knockdown of P2X7R plus P2X4R were performed by shRNA in macrophages and the result showed that P2X4R knockdown also partially inhibit the heme induced IL-1b secretion and double knockdown of P2X7R plus P2X4R almost completely depressed the IL-1b secretion (Fig. 3d). PubMed:24464629

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

p(MGI:P2rx4) positiveCorrelation a(CHEBI:heme) 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: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

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.