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Entity

Name
Wnt signaling pathway
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 4

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 6

act(p(HGNC:CHRM1)) increases bp(GO:"Wnt signaling pathway") View Subject | View Object

In addition to inhibiting Abeta generation, activation of M1 mAChR counteracts Abeta-induced neurotoxicity through the Wnt signaling pathway, as Abeta impairs the Wnt pathway and M1 mAChR stimulation inactivates GSK-3beta via PKC activation, stabilizes beta-catenin, and induces the expression of Wnt-targeting genes engrailed and cyclin-D1 for neuron survival PubMed:24590577

act(p(HGNC:GSK3B)) negativeCorrelation bp(GO:"Wnt signaling pathway") View Subject | View Object

In general, GSK-3β phosphorylation is inhibited through the canonical Wnt signalling pathway [5]. Wnt, binding to frizzled receptor, recruits dishevelled protein, which in turn antagonizes GSK-3β activity. PubMed:18494933

p(HGNC:DKK1) decreases bp(GO:"Wnt signaling pathway") View Subject | View Object

For example, ongoing inflammation can trigger various cell stress-response pathways, including overexpression of the secreted glycoprotein Dickopff-1 (DKK-1). DKK-1 up-regulates GSK-3β activity, promotes tau hyper-phosphorylation, NFT formation and neuronal degeneration. Thus, DKK-1 inhibits Wnt signalling in a manner similar to Aβ, and thereby fosters a self-sustaining feedback loop resulting in cellular injury PubMed:18494933

p(HGNC:S100B) decreases bp(GO:"Wnt signaling pathway") View Subject | View Object

In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3-beta phosphorylation and beta-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. PubMed:18494933

Appears in Networks:

p(HGNC:CTNNB1, pmod(Ph)) increases bp(GO:"Wnt signaling pathway") View Subject | View Object

In Xenopus, PP2A- B56 is involved in β -catenin dephosphorylation and degradation and its phosphorylation directs activation of the Wnt pathway [43]. PubMed:23454242

Out-Edges 3

bp(GO:"Wnt signaling pathway") decreases bp(HBP:neurotoxicity) View Subject | View Object

In addition to inhibiting Abeta generation, activation of M1 mAChR counteracts Abeta-induced neurotoxicity through the Wnt signaling pathway, as Abeta impairs the Wnt pathway and M1 mAChR stimulation inactivates GSK-3beta via PKC activation, stabilizes beta-catenin, and induces the expression of Wnt-targeting genes engrailed and cyclin-D1 for neuron survival PubMed:24590577

bp(GO:"Wnt signaling pathway") negativeCorrelation act(p(HGNC:GSK3B)) View Subject | View Object

In general, GSK-3β phosphorylation is inhibited through the canonical Wnt signalling pathway [5]. Wnt, binding to frizzled receptor, recruits dishevelled protein, which in turn antagonizes GSK-3β activity. PubMed:18494933

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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.