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Appears in Networks 2

In-Edges 1

a(CHEBI:"amyloid-beta") increases act(p(FPLX:TLR)) 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

Out-Edges 3

p(FPLX:TLR) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Aβ is cleared by receptor-mediated microglial phagocytosis and degradation, such as scavenger receptors, chemokine-like receptor 1, toll-like receptors, and G protein-coupled receptors including formyl peptide receptor 2 (Yu and Ye 2015) PubMed:29626319

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

act(p(FPLX:TLR)) increases p(HGNC:IL1B) 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

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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.