Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2019-05-15 22:27:13.462908
Authors
Sandra Spalek
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2019 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
12
Number Edges
27
Number Components
1
Network Density
0.204545454545455
Average Degree
2.25
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
mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0 33%
The autism/neuroprotection-linked ADNP/NAP regulate the excitatory glutamatergic synapse v1.0.0 33%
Activity-dependent neuroprotective protein deficiency models synaptic and developmental phenotypes of autism-like syndrome v1.0.0 33%
Heme Curation v0.0.1-dev 8%
The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0 8%
Alpha-synuclein oligomers: a new hope v1.0.0 8%
Abnormal Alzheimer-like phosphorylation of tau-protein by cyclin-dependent kinases cdk2 and cdk5 v1.0.0 8%
Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0 8%
Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 v1.0.0 8%
Molecular chaperones and regulation of tau quality control: strategies for drug discovery in tauopathies v1.0.0 8%

Sample Edges

a(PUBCHEM:9832404) increases complex(a(GO:microtubule), p(HGNC:ADNP)) View Subject | View Object

NAP has been shown to ameliorate Adnp deficiencies in the haploinsufficient mouse model [25], mechanistically by enhancing ADNP association with its microtubule and autophagy targets PubMed:30008470

a(PUBCHEM:9832404) increases act(p(HGNC:ADNP)) View Subject | View Object

These results indicate that restoration of ADNP function by NAP administration rescues the wild type phenotype of the Adnp+/− mice, by reversing the abnormal increase in alcohol intake seen in Adnp haploinsufficient female mice PubMed:30008470

Annotations
Gender
Female

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.