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p(FPLX:CHRM)

Equivalencies: 0 | Classes: 1 | Children: 0 | Explore

Entity

Name
CHRM
Namespace
FPLX
Namespace Version
20180917
Namespace URL
https://raw.githubusercontent.com/sorgerlab/famplex/e8ae9926ff95266032cb74f77973c84939bffbeb/export/famplex.belns

Appears in Networks 4

Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System v1.0.0

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

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

Neural Systems Governed by Nicotinic Acetylcholine Receptors: Emerging Hypotheses v1.0.0

In-Edges 11

complex(a(CHEBI:acetylcholine), p(FPLX:CHRM)) hasComponent p(FPLX:CHRM) View Subject | View Object

Appears in Networks:

a(CHEBI:"amyloid-beta") decreases act(p(FPLX:CHRM)) View Subject | View Object

Although Aβ peptides negatively alter the cholinergic system at multiple sites, including ACh synthesis, ACh release, and muscarinic receptors (157), the discovery that Aβ1−42 binds to α7 nAChRs with high affinity suggested the potential for a causal role of nAChRs in AD (159, 160). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:acetylcholine) increases act(p(FPLX:CHRM)) View Subject | View Object

When cholinergic neurons are depolarized, ACh is exocytosed from synaptic vesicles and released into the synaptic cleft, where it can activate both muscarinic and nicotinic receptors PubMed:26813123

Appears in Networks:

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

Appears in Networks:

a(MESH:"Quinuclidinyl Benzilate") 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

Appears in Networks:

complex(a(CHEBI:Muscarine), p(FPLX:CHRM)) hasComponent p(FPLX:CHRM) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:Muscarine), p(FPLX:CHRM)) increases act(p(FPLX:CHRM)) View Subject | View Object

The first selective agonist identified for muscarinic receptors was muscarine and, so far, there is no agonist available with a specific selectivity for one particular subtype of muscarinic receptor PubMed:26813123

Appears in Networks:

p(MGI:App, var("?")) decreases p(FPLX:CHRM) View Subject | View Object

In addition, quantitative autoradiography assay revealed that choline uptake was reduced in the hippocampus of these animals and that the expression of muscarinic and nicotinic cholinergic receptors was diminished PubMed:26813123

Appears in Networks:
Annotations
MeSH
Hippocampus

complex(a(CHEBI:nicotine), p(FPLX:CHRM)) hasComponent p(FPLX:CHRM) View Subject | View Object

Appears in Networks:

path(MESH:"Alzheimer Disease") decreases p(FPLX:CHRM) View Subject | View Object

Binding studies performed with the use of [3H]-nicotine and [3H]-ACh showed a significant reduction in nicotine and ACh binding sites in cerebral cortex of patients suffering from AD, demonstrating a decrease of both nAChR and mAChR populations (Gotti et al., 2006a; Paterson and Nordberg, 2000; Perry et al., 1981, 1985, 1987, 1988; Shimohama et al., 1986; Whitehouse et al., 1981, 1982, 1986) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

a(CHEBI:acetylcholine) increases act(p(FPLX:CHRM)) View Subject | View Object

We now realize that acetylcholine liberated from cholinergic nerve terminals often activates both nAChRs and muscarinic receptors PubMed:21482353

Appears in Networks:

Out-Edges 8

p(FPLX:CHRM) isA a(MESH:"Receptors, G-Protein-Coupled") View Subject | View Object

Appears in Networks:

p(FPLX:CHRM) regulates a(MESH:"Ion Channels") View Subject | View Object

Muscarinic receptors are G protein coupled receptors that are capable of modulating a wide variety of ion channels PubMed:26813123

Appears in Networks:

p(FPLX:CHRM) regulates act(a(MESH:"Calcium Channels")) View Subject | View Object

As a consequence, stimulation of ACh muscarinic receptors can promote the opening or closing of Ca2+, K+, or Cl- channels, which might facilitate either depolarization or hyperpolarization, depending on the cell type where these receptors are expressed PubMed:26813123

Appears in Networks:

p(FPLX:CHRM) regulates act(a(MESH:"Potassium Channels")) View Subject | View Object

As a consequence, stimulation of ACh muscarinic receptors can promote the opening or closing of Ca2+, K+, or Cl- channels, which might facilitate either depolarization or hyperpolarization, depending on the cell type where these receptors are expressed PubMed:26813123

Appears in Networks:

act(p(FPLX:CHRM)) decreases act(a(MESH:"Potassium Channels")) View Subject | View Object

Activation of muscarinic receptors can block various types of K+ currents by inhibiting many resting and voltage-gated K+ channels PubMed:26813123

Appears in Networks:

p(FPLX:CHRM) regulates act(a(MESH:"Chloride Channels")) View Subject | View Object

As a consequence, stimulation of ACh muscarinic receptors can promote the opening or closing of Ca2+, K+, or Cl- channels, which might facilitate either depolarization or hyperpolarization, depending on the cell type where these receptors are expressed PubMed:26813123

Appears in Networks:

act(p(FPLX:CHRM)) decreases bp(GO:"synaptic transmission, glutamatergic") View Subject | View Object

In addition to decreasing K+ currents, muscarinic receptors located at the presynaptic region can also inhibit GABAergic neurotransmission PubMed:26813123

Appears in Networks:

p(FPLX:CHRM) regulates bp(GO:cognition) View Subject | View Object

The neurotransmitter ACh binds to two families of receptors, nicotinic acetylcholine receptors (nAChRs) and muscarinic acetylcholine receptors (mAChRs). Both families of receptors regulate the cognitive processes mentioned above (Ghoneim and Mewaldt, 1977; Petersen, 1977; Sarter and Paolone, 2011), and are both affected in AD PubMed:25514383

Appears in Networks:

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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.