Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Appears in Networks 2

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

In-Edges 1

a(TAXONOMY:33113) increases a(CHEBI:atropine) View Subject | View Object

The metabotropic receptors are second messenger, G protein-coupled seven-transmembrane proteins. They are classically defined as being activated by muscarine, a toxin from the mushroom Amanita muscaria, and inhibited by atropine, a toxin from Atropa belladonna, a member of the nightshade family. Both toxins cross the blood-brain barrier poorly and were discovered primarily from their influences on postganglionic parasympathetic nervous system functions. Activation of muscarinic AChRs is relatively slow (milliseconds to seconds) and, depending on the subtypes present (M1- M5), they directly alter cellular homeostasis of phospholipase C, inositol trisphosphate, cAMP, and free calcium. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

Out-Edges 4

a(CHEBI:atropine) decreases act(p(HGNCGENEFAMILY:"Cholinergic receptors muscarinic")) View Subject | View Object

The metabotropic receptors are second messenger, G protein-coupled seven-transmembrane proteins. They are classically defined as being activated by muscarine, a toxin from the mushroom Amanita muscaria, and inhibited by atropine, a toxin from Atropa belladonna, a member of the nightshade family. Both toxins cross the blood-brain barrier poorly and were discovered primarily from their influences on postganglionic parasympathetic nervous system functions. Activation of muscarinic AChRs is relatively slow (milliseconds to seconds) and, depending on the subtypes present (M1- M5), they directly alter cellular homeostasis of phospholipase C, inositol trisphosphate, cAMP, and free calcium. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:atropine) decreases act(p(HGNCGENEFAMILY:"Cholinergic receptors muscarinic")) View Subject | View Object

Furthermore, pharmacological dissection of nicotine’s influence on cell cycle progression, apoptosis, and differentiation (43) indicate that alpha7 nAChRs expressed in keratynocytes are important. Other receptors are clearly involved in this process, since atropine, a muscarinic and sometimes nAChR inhibitor (531, 532), reduces cell adhesion through decreasing desmoligein expression. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Keratinocytes
Text Location
Review

a(CHEBI:atropine) decreases bp(GO:"cell adhesion") View Subject | View Object

Furthermore, pharmacological dissection of nicotine’s influence on cell cycle progression, apoptosis, and differentiation (43) indicate that alpha7 nAChRs expressed in keratynocytes are important. Other receptors are clearly involved in this process, since atropine, a muscarinic and sometimes nAChR inhibitor (531, 532), reduces cell adhesion through decreasing desmoligein expression. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Keratinocytes
Text Location
Review

a(CHEBI:atropine) decreases act(p(FPLX:CHRM)) View Subject | View Object

The two best known muscarinic receptor antagonists are atropine and quinuclidinyl benzilate, which block all muscarinic receptors PubMed:26813123

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.