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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:05.216954
Authors
Rana Aldisi
Contact
charles.hoyt@scai.fraunhofer.de
Description
This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
23
Number Edges
50
Number Components
1
Network Density
0.0988142292490119
Average Degree
2.17391304347826
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
Tau Modifications v1.9.5 52%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 50%
TAU and Interaction Partners v1.2.5 35%
Alzheimer's Disease: Targeting the Cholinergic System v1.0.0 35%
Tau in physiology and pathology v1.0.0 30%
Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0 30%
The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0 30%
Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer’s disease brain v1.0.1 29%
Protein phosphatase 2A dysfunction in Alzheimer’s disease v1.0.0 26%
Alzheimer’s disease and the autophagic-lysosomal system v1.0.0 26%

Sample Edges

a(CHEBI:LY294002) decreases p(HGNC:MAPT, pmod(Ph, Thr, 231)) View Subject | View Object

Interestingly, we found that tau hyperphosphorylation at Thr231 was completely blocked by the Src family tyrosine kinase inhibitor, 4-amino-5-(4- chlorophenyl)-7(t-butyl)pyrazol(3,4-d)pyramide (PP1), and by the phosphatidylinositol 3-kinase inhibitor, LY294002 (Fig. 5). PubMed:17403556

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Text Location
Results

a(CHEBI:LY294002) decreases bp(GO:"signal transduction") View Subject | View Object

Inhibition occurred even though ADDLs were still bound to cell surfaces, indicating that those kinases are involved in signal transduction coupling between ADDL binding and tau hyperphosphorylation. PubMed:17403556

Annotations
Text Location
Results

Sample Nodes

path(MESH:"Alzheimer Disease")

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

p(HGNC:MAPT)

In-Edges: 477 | Out-Edges: 480 | Classes: 11 | Children: 27 | Explore Neighborhood | Download JSON

p(HGNC:MAPT, pmod(Ph))

In-Edges: 201 | Out-Edges: 71 | Classes: 1 | Children: 4 | 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.