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Activity-dependent neuroprotective protein deficiency models synaptic and developmental phenotypes of autism-like syndrome 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-05-15 22:27:12.142780
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
66
Number Edges
183
Number Components
1
Network Density
0.0426573426573427
Average Degree
2.77272727272727
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 autism/neuroprotection-linked ADNP/NAP regulate the excitatory glutamatergic synapse v1.0.0 35%
Activity-dependent neuroprotective protein (ADNP) is an alcohol-responsive gene and negative regulator of alcohol consumption in female mice v1.0.0 33%
Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice v1.0.0 18%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 17%
Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0 15%
Anti-aggregant tau mutant promotes neurogenesis v1.0.0 15%
mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0 14%
Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0 13%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 12%
Tau Modifications v1.9.5 12%

Sample Edges

a(GO:"actin cytoskeleton") association p(HGNC:MTOR) View Subject | View Object

Likewise, mechanistic target of rapamycin (Mtor), which has been linked to cellular regulation, protein translation, autophagy, and the actin cytoskeleton (43–45), was also found to be regulated by ADNP and NAP PubMed:30106381

act(a(GO:synapse)) association p(HGNC:ADNP) View Subject | View Object

Additionally, given that ADNP and NAP are linked with autophagy (13), cell adhesion (35), immune response (36), autism (6, 13, 15, 17, 27), and synapse-related processes (6), the analysis included several representative genes pertaining to these processes PubMed:30106381

act(a(GO:synapse)) association a(PUBCHEM:9832404) View Subject | View Object

Additionally, given that ADNP and NAP are linked with autophagy (13), cell adhesion (35), immune response (36), autism (6, 13, 15, 17, 27), and synapse-related processes (6), the analysis included several representative genes pertaining to these processes PubMed:30106381

a(PUBCHEM:9832404) increases a(GO:"dendritic spine") View Subject | View Object

The measurements showed similar patterns in both tested brain areas, with Adnp deficiency resulting in substantial decreases in spine density (male and female mice) and increases in PSD95-asymmetric shaft synapses (males only, as indicated by increased localization of PSD95 in dendritic shafts rather than spines), which were all rescued by NAP treatment. PubMed:30106381

Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Cerebral Cortex
MeSH
Pyramidal Cells
Gender
Male
Gender
Female

a(PUBCHEM:9832404) increases a(GO:"dendritic spine") View Subject | View Object

In hippocampal CA1 pyramidal cells, all dendritic spine subtypes were reduced in the Adnp+/– mice, except for the thin spines observed in males. The spine loss was rescued by NAP treatment, except for the stubby spines seen in males (Supplemental Figure 1). PubMed:30106381

Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Pyramidal Cells
Gender
Male
Gender
Female

Sample Nodes

bp(GO:"cell adhesion")

In-Edges: 11 | Out-Edges: 5 | Explore Neighborhood | Download JSON

bp(GO:"immune response")

In-Edges: 7 | Out-Edges: 5 | Explore Neighborhood | Download JSON

bp(GO:learning)

In-Edges: 52 | Out-Edges: 24 | Explore Neighborhood | Download JSON

bp(GO:memory)

In-Edges: 112 | Out-Edges: 33 | Explore Neighborhood | Download JSON

path(MESH:"Alzheimer Disease")

In-Edges: 536 | Out-Edges: 704 | Classes: 5 | 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.