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complex(p(FPLX:"G_protein"), p(HGNC:CHRM1))

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Components

Appears in Networks 1

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

In-Edges 1

a(CHEBI:"amyloid-beta") decreases complex(p(FPLX:"G_protein"), p(HGNC:CHRM1)) View Subject | View Object

In fact, Abeta has been shown to induce the uncoupling of M1 mAChR from G-protein, antagonizing the function of M1 mAChR under the pathological conditions of AD[96, 97]. Such an uncoupling may result in decreased signal transduction, reduced levels of sAPPalpha, and increased production of Abeta, triggering a vicious cycle. PubMed:24590577

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 5

complex(p(FPLX:"G_protein"), p(HGNC:CHRM1)) hasComponent p(FPLX:"G_protein") View Subject | View Object

Appears in Networks:

complex(p(FPLX:"G_protein"), p(HGNC:CHRM1)) hasComponent p(HGNC:CHRM1) View Subject | View Object

Appears in Networks:

complex(p(FPLX:"G_protein"), p(HGNC:CHRM1)) increases a(HBP:"sAPP-alpha") View Subject | View Object

In fact, Abeta has been shown to induce the uncoupling of M1 mAChR from G-protein, antagonizing the function of M1 mAChR under the pathological conditions of AD[96, 97]. Such an uncoupling may result in decreased signal transduction, reduced levels of sAPPalpha, and increased production of Abeta, triggering a vicious cycle. PubMed:24590577

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(p(FPLX:"G_protein"), p(HGNC:CHRM1)) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

In fact, Abeta has been shown to induce the uncoupling of M1 mAChR from G-protein, antagonizing the function of M1 mAChR under the pathological conditions of AD[96, 97]. Such an uncoupling may result in decreased signal transduction, reduced levels of sAPPalpha, and increased production of Abeta, triggering a vicious cycle. PubMed:24590577

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(p(FPLX:"G_protein"), p(HGNC:CHRM1)) increases bp(GO:"signal transduction") View Subject | View Object

In fact, Abeta has been shown to induce the uncoupling of M1 mAChR from G-protein, antagonizing the function of M1 mAChR under the pathological conditions of AD[96, 97]. Such an uncoupling may result in decreased signal transduction, reduced levels of sAPPalpha, and increased production of Abeta, triggering a vicious cycle. PubMed:24590577

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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.