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The role of inflammasome in Alzheimer’s disease 1.0.3

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:51.326805
Authors
Sandra Spalek
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
70
Number Edges
166
Number Components
2
Network Density
0.0343685300207039
Average Degree
2.37142857142857
Number Citations
1
Number BEL Errors
0

Content Statistics

Network Overlap

The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.

Network Overlap
Inflammasome activation and innate immunity in Alzheimer’s disease v1.0.2 29%
Inflammasome Involvement in Alzheimer’s Disease v1.0.0 26%
Activation and regulation of the inflammasomes v1.0.0 26%
A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0 24%
Heme Curation v0.0.1-dev 21%
In Vivo and In Vitro Characterization of Antalarmin, a Nonpeptide Corticotropin-Releasing Hormone (CRH) Receptor Antagonist: Suppression of Pituitary ACTH Release and Peripheral Inflammation v1.0.0 20%
Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice v1.0.0 18%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 17%
Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0 16%
Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0 16%

Sample Edges

complex(GO:"inflammasome complex") hasComponent p(HGNC:CASP1) View Subject | View Object

a(CHEBI:"amyloid-beta") increases act(complex(GO:"inflammasome complex")) View Subject | View Object

Activators include bacteria, virus, fungus, protoza, microbial proteins, crystalline urea, RNA, Alum, ATP, potassium efflux, fatty acids, Aβ, and most recently, degraded mitochondrial DNA (Liu et al., 2013a; Mathew et al., 2012; Schmidt and Lenz, 2012) PubMed:24561250

Annotations
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph

a(CHEBI:"amyloid-beta") increases bp(GO:phagocytosis) View Subject | View Object

Phagocytosis and subsequent lysosomal damage trigger by Aβ initiate the activation of the NLRP3 inflammasome in the microglia (Halle et al., 2008) PubMed:24561250

Annotations
Cell Ontology (CL)
microglial cell
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph

a(CHEBI:"amyloid-beta") decreases a(GO:lysosome) View Subject | View Object

Phagocytosis and subsequent lysosomal damage trigger by Aβ initiate the activation of the NLRP3 inflammasome in the microglia (Halle et al., 2008) PubMed:24561250

Annotations
Cell Ontology (CL)
microglial cell
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Endosomal lysosomal subgraph

a(CHEBI:"fatty acid") increases act(complex(GO:"inflammasome complex")) View Subject | View Object

Activators include bacteria, virus, fungus, protoza, microbial proteins, crystalline urea, RNA, Alum, ATP, potassium efflux, fatty acids, Aβ, and most recently, degraded mitochondrial DNA (Liu et al., 2013a; Mathew et al., 2012; Schmidt and Lenz, 2012) PubMed:24561250

Annotations
Confidence
High

Sample Nodes

a(CHEBI:"amyloid-beta")

In-Edges: 423 | Out-Edges: 245 | Children: 5 | Explore Neighborhood | Download JSON

bp(GO:"inflammatory response")

In-Edges: 55 | Out-Edges: 24 | Explore Neighborhood | Download JSON

bp(GO:aging)

In-Edges: 27 | Out-Edges: 61 | Explore Neighborhood | Download JSON

bp(GO:cognition)

In-Edges: 111 | Out-Edges: 35 | Explore Neighborhood | Download JSON

bp(GO:learning)

In-Edges: 52 | Out-Edges: 24 | Explore Neighborhood | Download JSON

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.