Upload at 2019-03-15 15:44:05.162184
Esther Wollert
CC BY 4.0
Copyright © 2019 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
Number Edges
Number Components
Network Density
Average Degree
Number Citations
Number BEL Errors

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

Cell Ontology (CL)
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

Experimental Factor Ontology (EFO)

Sample Nodes


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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.