Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:21:03.264505
Authors
Esther Wollert
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
94
Number Edges
160
Number Components
2
Network Density
0.0183024479524136
Average Degree
1.70212765957447
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
A chaperome subnetwork safeguards proteostasis in aging and neurodegenerative disease. v1.0.0 38%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 33%
Model systems of protein-misfolding diseases reveal chaperone modifiers of proteotoxicity v1.0.0 33%
Protein aggregation can inhibit clathrin-mediated endocytosis by chaperone competition v1.0.0 31%
Molecular Chaperone Functions in Protein Folding and Proteostasis v1.0.0 29%
Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0 27%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 25%
Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. v1.0.0 23%
The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0 20%
Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.1 19%

Sample Edges

a(CHEBI:"amyloid-beta") decreases act(p(FPLX:Proteasome)) View Subject | View Object

Experiments examining the effects of Aβ on proteasomal activity in vitro revealed an inhibitory effect on the chymotrypsin-like properties of the 20S core (73), consistent with observations of impaired proteasome function in AD patient brains (74). PubMed:25784053

a(CHEBI:chloroquine) decreases bp(GO:autophagy) View Subject | View Object

Reduced levels of lipofuscin, LC3, and p62 have been observed in motor neurons of SOD1(G85R) mice (92). Treatment with the autophagy inhibitor chloroquine restored lipofuscin, LC3, and p62 levels in motor neurons, suggesting that mutant SOD1 causes hyperactive autophagy in mice (92). PubMed:25784053

Annotations
Cell Ontology (CL)
motor neuron

a(CHEBI:chloroquine) increases a(CHEBI:"N-retinylidene-N-retinylethanolamine") View Subject | View Object

Reduced levels of lipofuscin, LC3, and p62 have been observed in motor neurons of SOD1(G85R) mice (92). Treatment with the autophagy inhibitor chloroquine restored lipofuscin, LC3, and p62 levels in motor neurons, suggesting that mutant SOD1 causes hyperactive autophagy in mice (92). PubMed:25784053

Annotations
Cell Ontology (CL)
motor neuron

Sample Nodes

a(CHEBI:"amyloid-beta")

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

path(MESH:"Alzheimer Disease")

In-Edges: 536 | Out-Edges: 704 | Classes: 5 | Explore Neighborhood | Download JSON

a(CHEBI:sirolimus)

In-Edges: 8 | Out-Edges: 50 | 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.