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Anatabine lowers Alzheimer's Aβ production in vitro and in vivo 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-03-15 15:36:31.152263
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
20
Number Edges
37
Number Components
1
Network Density
0.0973684210526316
Average Degree
1.85
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 Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0 40%
Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0 40%
Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0 35%
Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0 35%
Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0 30%
Effects of peptides derived from BACE1 catalytic domain on APP processing v1.0.0 30%
Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0 30%
Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. v1.0.0 25%
albuquerque2009 v1.0.0 25%
Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0 25%

Sample Edges

p(HGNC:RELA) hasVariant p(HGNC:RELA, pmod(Ph)) View Subject | View Object

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

Anatabine dose dependently inhibited Aβ1–40 and Aβ1–42 with an approximate half maximal inhibitory concentration of 640 μg/ml for both Aβ1–40 and Aβ1–42 (Fig. 2). PubMed:21958873

Annotations
Experimental Factor Ontology (EFO)
CHO cell

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

We then tested the impact of anatabine on sAPPα and sAPPβ production using 7W CHO cells and observed that anatabine inhibits sAPPβ secretion without impacting sAPPα suggesting that anatabine is preventing the β-cleavage of APP (Fig. 4). PubMed:21958873

Annotations
Experimental Factor Ontology (EFO)
CHO cell

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

A significant reduction in the accumulation of brain soluble and insoluble Aβ1–40 and Aβ1–42 was observed following four days of treatment with 2 mg/kg of anatabine (Fig. 9). PubMed:21958873

Annotations
MeSH
Brain

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Anatabine dose dependently inhibited Aβ1–40 and Aβ1–42 with an approximate half maximal inhibitory concentration of 640 μg/ml for both Aβ1–40 and Aβ1–42 (Fig. 2). PubMed:21958873

Annotations
Experimental Factor Ontology (EFO)
CHO cell

Sample Nodes

a(CHEBI:"amyloid-beta")

In-Edges: 423 | Out-Edges: 245 | Children: 5 | Explore Neighborhood | Download JSON

a(CHEBI:"amyloid-beta polypeptide 40")

In-Edges: 23 | Out-Edges: 5 | Classes: 1 | Explore Neighborhood | Download JSON

p(HGNC:BACE1)

In-Edges: 65 | Out-Edges: 39 | Explore Neighborhood | Download JSON

p(HBP:"sAPP-alpha")

In-Edges: 3 | Out-Edges: 2 | Explore Neighborhood | Download JSON

p(HBP:"sAPP-beta")

In-Edges: 10 | Out-Edges: 1 | 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.