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  3. complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN))

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN))

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Components

Appears in Networks 2

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0

In-Edges 2

a(HBP:"PTI-125") decreases complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) View Subject | View Object

A novel molecule called PTI-125 was used to interfere with the interaction of FLNA and alpha7. The treatment with PTI-125 prevents FLNA binding to alpha7 and as consequence reduces the affinity of Abeta for nAChRs, attenuating the toxic effect of Abeta (Wang et al., 2012) PubMed:25514383

Appears in Networks:

bp(GO:"neuron cellular homeostasis") association complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) View Subject | View Object

It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383

Appears in Networks:

Out-Edges 6

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) hasComponent a(CHEBI:"amyloid-beta") View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) increases bp(GO:"intracellular signal transduction") View Subject | View Object

However, it is clear that nAChR-Aß interaction initiates intracellular signalling implicating a set of transduction cascades PubMed:25514383

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) decreases bp(MESH:"Cell Survival") View Subject | View Object

On the other hand, an opposite effect was shown with Abeta-nAChR interaction being responsible for inhibition of survival pathways PubMed:25514383

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) association bp(GO:"neuron cellular homeostasis") View Subject | View Object

It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) increases path(MESH:"Memory Disorders") View Subject | View Object

The hAPP-SLA transduction in DG did not induce a memory deficit in beta2 KO, meaning that the Abeta/beta2-nAChR interaction is required to drive the memory deficit in this model PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

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.