Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:17.385690
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
95
Number Edges
191
Number Components
3
Network Density
0.0213885778275476
Average Degree
2.01052631578947
Number Citations
1
Number BEL Errors
0

Content Statistics

ProteinBiologicalProcessComplexAbundancePathology05101520253035Nodes (95)
associationdecreasesincreaseshasComponentisAhasVariantregulatespositiveCorrelation05101520253035404550Edges (191)
MolecularActivitiesDegradations00.511.522.533.544.555.566.5Transformations (9)
pmodhgvs01234567Variants (9)
HGNCMESHGOHBPFPLXCHEBIPUBCHEM051015202530Namespace Usage (7)
HSP90AgingSTUB1AlzheimerDiseaseMAPTTauaggregatesAHSA1HSP90AB1PPIDHSP90AA1FKBP4PTGES3TauopathiesImmunophilins05101520253035404550Node Degrees
AlzheimerDiseaseTauopathiesProteinAggregation,PathologicalCysticFibrosisNeurodegenerativeDiseasesNeoplasmMetastasisHuntingtonDiseaseParkinsonDiseaseNeoplasmsChronicTraumaticEncephalopathyPickDisease ofthe BrainSupranuclear Palsy,Progressive012345678910111213Pathologies
2016201720182019-0.100.10.20.30.40.50.60.70.80.911.1Publication Years

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
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 50%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 50%
Tau Trimers Are the Minimal Propagation Unit Spontaneously Internalized to Seed Intracellular Aggregation v1.0.0 45%
Pseudophosphorylation of tau at S422 enhances SDS-stable dimer formation and impairs both anterograde and retrograde fast axonal transport. v1.0.0 33%
Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0 29%
A chaperome subnetwork safeguards proteostasis in aging and neurodegenerative disease. v1.0.0 28%
Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro v1.0.0 27%
Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer’s disease brain v1.0.1 24%
Molecular chaperones and regulation of tau quality control: strategies for drug discovery in tauopathies v1.0.0 23%
Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.1 22%

Sample Edges

Sample Nodes

bp(GO:memory)

In-Edges: 112 | Out-Edges: 33 | Explore Neighborhood | Download JSON

path(MESH:"Alzheimer Disease")

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

bp(MESH:Aging)

In-Edges: 10 | Out-Edges: 65 | 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.