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Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-05-15 22:26:59.266336
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
20
Number Edges
35
Number Components
1
Network Density
0.0921052631578947
Average Degree
1.75
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
Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0 65%
Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0 50%
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 40%
Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0 30%
Identification of a novel aspartic protease (Asp 2) as beta-secretase v1.0.0 30%
Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0 30%
Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0 30%
APP processing in Alzheimer's disease v1.0.1 25%
albuquerque2009 v1.0.0 25%
M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0 25%

Sample Edges

a(CHEBI:"acetylsalicylic acid") decreases r(HGNC:BACE1) View Subject | View Object

Compared to controls, TNF-a treatment resulted in significant increase in luciferase activity in the cells transfected with the human BACE1 promoter pB1P- N1 plasmid (p<0.005) and addition of aspirin in- hibited the BACE1 transcriptional activation induced by TNF-a (p<0.005 relative to TNF-a and p>0.05 relative to controls) (Fig. 6a). PubMed:21329555

a(CHEBI:"acetylsalicylic acid") decreases r(HGNC:BACE1) View Subject | View Object

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

a(CHEBI:"acetylsalicylic acid") isA a(MESH:"Anti-Inflammatory Agents, Non-Steroidal") View Subject | View Object

a(CHEBI:ibuprofen) isA a(MESH:"Anti-Inflammatory Agents, Non-Steroidal") View Subject | View Object

a(CHEBI:ibuprofen) decreases r(HGNC:BACE1) View Subject | View Object

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

Sample Nodes

a(CHEBI:"amyloid-beta")

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

path(MESH:"Alzheimer Disease")

In-Edges: 536 | Out-Edges: 704 | Classes: 5 | Explore Neighborhood | Download JSON

path(MESH:Inflammation)

In-Edges: 83 | Out-Edges: 41 | Explore Neighborhood | Download JSON

p(HGNC:APP)

In-Edges: 106 | Out-Edges: 69 | Explore Neighborhood | Download JSON

p(HGNC:BACE1)

In-Edges: 65 | Out-Edges: 39 | 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.