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Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems 1.0.1

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charles.hoyt@scai.fraunhofer.de at 2019-05-15 22:27:15.316465
Authors
Esther Wollert
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2019 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
27
Number Edges
52
Number Components
1
Network Density
0.0740740740740741
Average Degree
1.92592592592593
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 50%
The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0 41%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 38%
Molecular chaperones and regulation of tau quality control: strategies for drug discovery in tauopathies v1.0.0 37%
Tau Modifications v1.9.5 37%
Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0 35%
Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. v1.0.0 33%
Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1 33%
Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0 30%
Alzheimer’s disease and the autophagic-lysosomal system v1.0.0 30%

Sample Edges

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

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, pmod(Ph, Ser, 202), pmod(Ph, Thr, 205)) View Subject | View Object

a(CHEBI:"(-)-anisomycin") decreases bp(GO:translation) View Subject | View Object

Conversely, treatment with protein translation inhibitors, cycloheximide or anisomycin, alone (Fig. S8A and B) almost completely abrogated MAPT missorting (schematic in Fig. 2E). These results suggest that the dendritic MAPT is locally generated. PubMed:30145931

a(CHEBI:"(-)-anisomycin") decreases p(HGNC:MAPT, loc(MESH:Dendrites)) View Subject | View Object

Conversely, treatment with protein translation inhibitors, cycloheximide or anisomycin, alone (Fig. S8A and B) almost completely abrogated MAPT missorting (schematic in Fig. 2E). These results suggest that the dendritic MAPT is locally generated. PubMed:30145931

a(CHEBI:"alpha,alpha-trehalose") increases bp(GO:autophagy) View Subject | View Object

Our previous study [23] had shown that trehalose induces autophagy in primary neurons and in an N2a cell model of tauopathy, and efficiently reduces the level of MAPT and MAPT aggregation. PubMed:30145931

Annotations
MeSH
Neurons

Sample Nodes

bp(GO:aging)

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

path(MESH:"Alzheimer Disease")

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

a(MESH:"Dendritic Spines")

In-Edges: 23 | Out-Edges: 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(HBP:hyperphosphorylation))

In-Edges: 66 | Out-Edges: 47 | 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.