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bp(GO:"amyloid-beta formation")

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Entity

Name
amyloid-beta formation
Namespace
go
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/go-names.belns

Appears in Networks 2

A role for APP in Wnt signalling links synapse loss with β-amyloid production. v1.0.0

The role of inflammasome in Alzheimer’s disease v1.0.3

In-Edges 5

bp(GO:"Wnt signaling pathway, planar cell polarity pathway") positiveCorrelation bp(GO:"amyloid-beta formation") View Subject | View Object

Comparison of signalling activity and Aβ production under each of the different conditions showed clearly that Aβ production was negatively correlated with Wnt-β-catenin signalling activity (Fig. 2d) and positively correlated with Wnt-PCP signalling (Fig. 2e). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

bp(GO:"canonical Wnt signaling pathway") negativeCorrelation bp(GO:"amyloid-beta formation") View Subject | View Object

Comparison of signalling activity and Aβ production under each of the different conditions showed clearly that Aβ production was negatively correlated with Wnt-β-catenin signalling activity (Fig. 2d) and positively correlated with Wnt-PCP signalling (Fig. 2e). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

p(HGNC:DKK1) increases bp(GO:"amyloid-beta formation") View Subject | View Object

Notably, in parallel with the protective effect of fasudil on synapses (Fig. 3e, f), treatment with fasudil reversed the stimulatory effects of Dkk1 on Aβ production (Fig. 3g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

p(MGI:Casp1) increases bp(GO:"amyloid-beta formation") View Subject | View Object

In support, knockout of NLRP3 and caspase-1 have been shown to suppress amyloidogenesis and neuropathology, and improve cognition in AD transgenic mice (Heneka et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph

p(MGI:Nlrp3) increases bp(GO:"amyloid-beta formation") View Subject | View Object

In support, knockout of NLRP3 and caspase-1 have been shown to suppress amyloidogenesis and neuropathology, and improve cognition in AD transgenic mice (Heneka et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph

Out-Edges 2

bp(GO:"amyloid-beta formation") negativeCorrelation bp(GO:"canonical Wnt signaling pathway") View Subject | View Object

Comparison of signalling activity and Aβ production under each of the different conditions showed clearly that Aβ production was negatively correlated with Wnt-β-catenin signalling activity (Fig. 2d) and positively correlated with Wnt-PCP signalling (Fig. 2e). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

bp(GO:"amyloid-beta formation") positiveCorrelation bp(GO:"Wnt signaling pathway, planar cell polarity pathway") View Subject | View Object

Comparison of signalling activity and Aβ production under each of the different conditions showed clearly that Aβ production was negatively correlated with Wnt-β-catenin signalling activity (Fig. 2d) and positively correlated with Wnt-PCP signalling (Fig. 2e). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

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.