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Nuclear receptors as therapeutic targets for Alzheimer's disease. 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:16:47.781611
Authors
Esther Wollert
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2012-2018 Fraunhofer Institute SCAI, All rights reserved
Number Nodes
83
Number Edges
169
Number Components
4
Network Density
0.0248310314428445
Average Degree
2.03614457831325
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
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 33%
Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. v1.0.0 30%
Identification of a novel aspartic protease (Asp 2) as beta-secretase v1.0.0 30%
Effects of peptides derived from BACE1 catalytic domain on APP processing v1.0.0 30%
Posiphen as a candidate drug to lower CSF amyloid precursor protein, amyloid-b peptide and s levels: target engagement, tolerability and pharmacokinetics in humans v0.1.0 27%
Inflammasome activation and innate immunity in Alzheimer’s disease v1.0.2 25%
Anatabine lowers Alzheimer's Aβ production in vitro and in vivo v1.0.0 25%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 25%
Inflammasome Involvement in Alzheimer’s Disease v1.0.0 24%
Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0 24%

Sample Edges

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

a(CHEBI:"GW 3965") directlyIncreases act(p(HGNC:NR1H3)) View Subject | View Object

Importantly, this study utilized the LXR agonist, GW3965, to activate the LXRs and induce the expression of both ApoE and ABCA1. PubMed:21718217

Annotations
Confidence
High

a(CHEBI:"GW 3965") increases act(p(HGNC:NR1H3)) View Subject | View Object

Similarly, stimulation of microglia with the LXR agonist, GW3965, acts simultaneously to suppress inflammation and promote fibrillar Ab stimulated phagocytosis [47]. PubMed:21718217

Annotations
Confidence
Medium

a(CHEBI:"GW 3965") increases p(HGNC:APOE) View Subject | View Object

Importantly, this study utilized the LXR agonist, GW3965, to activate the LXRs and induce the expression of both ApoE and ABCA1. PubMed:21718217

Annotations
Confidence
High

a(CHEBI:"GW 3965") increases p(HGNC:ABCA1) View Subject | View Object

Importantly, this study utilized the LXR agonist, GW3965, to activate the LXRs and induce the expression of both ApoE and ABCA1. PubMed:21718217

Annotations
Confidence
High

Sample Nodes

a(CHEBI:"amyloid-beta")

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

a(HBP:HBP00018)

In-Edges: 35 | Out-Edges: 8 | Explore Neighborhood | Download JSON

a(MESH:Macrophages)

In-Edges: 6 | Out-Edges: 2 | Explore Neighborhood | Download JSON

bp(GO:cognition)

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

bp(GO:memory)

In-Edges: 112 | Out-Edges: 33 | 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.