Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2019-03-15 15:44:05.162184
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
13
Number Edges
15
Number Components
2
Network Density
0.0961538461538462
Average Degree
1.15384615384615
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
The Biology of Proteostasis in Aging and Disease v1.0.0 31%
Alzheimer’s disease and the autophagic-lysosomal system v1.0.0 31%
The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0 23%
The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0 23%
Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0 23%
mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0 15%
Heme Curation v0.0.1-dev 15%
A chaperome subnetwork safeguards proteostasis in aging and neurodegenerative disease. v1.0.0 15%
A Quantitative Chaperone Interaction Network Reveals the Architecture of Cellular Protein Homeostasis Pathways v1.0.0 15%
Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0 15%

Sample Edges

a(HBP:"Q82 aggregates") decreases bp(GO:"clathrin-dependent endocytosis") View Subject | View Object

However, CME was substantially reduced in cells con- taining Q82 aggregates (Fig. 1 B , arrows), with quantification of internalized transferrin fluorescence showing a 63 ± 11% reduction in aggregate-containing cells compared with cells expressing soluble Q19 or Q82 (Fig. 1 C ). PubMed:24706768

a(HBP:"huntingtin aggregates") decreases bp(GO:"clathrin-dependent endocytosis") View Subject | View Object

CME inhibition was also observed in cells containing aggregated forms of polyQ- expanded Htt exon 1 (Htt Q53); these cells exhibited 50 ± 15% reduced levels of internalized transferrin compared with cells with soluble Htt Q23 or Htt Q53 protein (Fig. S2 A–C ). PubMed:24706768

a(HBP:"huntingtin aggregates") decreases bp(GO:"clathrin-dependent endocytosis") View Subject | View Object

In contrast, there was a marked reduction in CME in neurons containing mutant Htt exon 1 Q73-CFP aggregates compared with nonexpressing cells (Fig. 5 B , Center ; quantification in Fig. 5 D ); PubMed:24706768

Annotations
Cell Ontology (CL)
neuron
MeSH
Huntington Disease

a(HBP:"polyQ aggregates") decreases act(p(HGNC:DNAJB1)) View Subject | View Object

It has been proposed that such an imbalance may trigger the onset of many neurodegenerative diseases (10, 26), and recent studies report that polyglutamine (polyQ)-based aggregates can se- quester and inhibit the function of a low-abundance cochaper- one, Sis1p/DNAJB1, in protein degradation (27). PubMed:24706768

a(HBP:"polyQ aggregates") decreases bp(GO:endocytosis) View Subject | View Object

Previous studies have shown that ag- gregation of expanded polyQ negatively affects endocytosis in yeast and in human HEK 293 cells (34). PubMed:24706768

Annotations
Experimental Factor Ontology (EFO)
HEK293

Sample Nodes

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.