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p(HGNC:CHRNB4)

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

Entity

Name
CHRNB4
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 10

albuquerque2009 v1.0.0

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

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. 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

NACHO Mediates Nicotinic Acetylcholine Receptor Function throughout the Brain v1.0.0

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

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Chaperoning α7 neuronal nicotinic acetylcholine receptors v1.0.0

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

In-Edges 15

complex(a(HBP:"kappa-Bungarotoxin"), p(HGNC:CHRNB4)) hasComponent p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

complex(a(HBP:"kappa-Bungarotoxin"), p(HGNC:CHRNB4)) decreases act(p(HGNC:CHRNB4)) View Subject | View Object

Such toxins are not limited to the muscle receptor as seen in the Taiwanese krate snake. This snake produces “neuronal bungarotoxin” (also referred to as 3.1 toxin or kappa-bungarotoxin; Ref. 286), which preferentially binds to and inactivates neuronal nAChRs that contain the alpha3 and beta4 subunits. In this case, the specificity of the toxin appears to in part be controlled by the subtype of beta nAChR subunit; beta2-containing nAChRs are less sensitive than beta4-containing nAChRs to inhibition by neuronal BGT. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

complex(p(HGNC:CHRNA3), p(HGNC:CHRNA5), p(HGNC:CHRNB4)) hasComponent p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

path(MESH:"Drug Tolerance") association p(HGNC:CHRNB4) View Subject | View Object

In summary, while nicotine-induced upregulation requires at least the beta2 nAChR subunit, development of tolerance to nicotine requires neither the beta2 nor the alpha7 nAChR subunit; instead, it appears to be modulated by a beta4-containing nAChR and to require an alpha4-containing nAChR. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

complex(p(HGNC:CHRNA3), p(HGNC:CHRNB4)) hasComponent p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

path(MESH:"Alzheimer Disease") decreases p(HGNC:CHRNB4) View Subject | View Object

Thus, in brains from patients with AD and in neurons responding to exogenously applied Abeta, there is a reduction in expression of nAChR subunits, especially alpha4, alpha7, beta4, and possibly alpha3. Although AD may also involve changes in expression of other ligand-gated ion channels— for example, the expression of NMDA receptors (Bi and Sze, 2002; Jacob et al., 2007), alpha-amino-3-hydroxy- 5-methyl-4-isoxazolepropionic acid receptors (Jacob et al., 2007), and beta3 GABA receptor subunits are all reduced (Mizukami et al., 1998)—there is abundant evidence of a loss of nAChR subunits in AD possibly caused by the actions of Abeta. PubMed:19293145

Appears in Networks:
Annotations
MeSH
Brain

p(FPLX:CHRN) hasMember p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

p(GFAM:"Cholinergic receptors nicotinic subunits") hasMember p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

act(a(CHEBI:nicotine)) association p(HGNC:CHRNB4) View Subject | View Object

Moreover, nAChRs containing β4, α2 and α5 in the habenulo-interpeduncular systems are necessary for nicotine withdrawal in mice107 PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

path(MESH:Craving) association p(HGNC:CHRNB4) View Subject | View Object

β4 deletion abolishes withdrawal signs in the mouse208, and α3 and β4 are also present in the PNS, supporting the view that they might be directly involved in craving and relapse — an area that is largely unexplored in the development of medications to assist with smoking cessation. PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

path(MESH:Recurrence) association p(HGNC:CHRNB4) View Subject | View Object

β4 deletion abolishes withdrawal signs in the mouse208, and α3 and β4 are also present in the PNS, supporting the view that they might be directly involved in craving and relapse — an area that is largely unexplored in the development of medications to assist with smoking cessation. PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

complex(p(HGNC:CHRNB4), p(HGNC:RIC3)) hasComponent p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

bp(HBP:"habenulo-interpeduncular pathway") increases p(HGNC:CHRNB4, loc(MESH:"Central Nervous System")) View Subject | View Object

The Hb-IPN system expresses the highest levels and va- riety of nAChR subunits and subtypes in mammalian brain [85], and is the only central system expressing high levels of α3, β4 and α5 subunits. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

complex(p(HGNC:CHRNA3), p(HGNC:CHRNA5), p(HGNC:CHRNB2), p(HGNC:CHRNB4)) hasComponent p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CHRNA5), p(HGNC:CHRNA7), p(HGNC:CHRNB2), p(HGNC:CHRNB3), p(HGNC:CHRNB4)) hasComponent p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

Out-Edges 6

p(HGNC:CHRNB4) association path(MESH:"Drug Tolerance") View Subject | View Object

In summary, while nicotine-induced upregulation requires at least the beta2 nAChR subunit, development of tolerance to nicotine requires neither the beta2 nor the alpha7 nAChR subunit; instead, it appears to be modulated by a beta4-containing nAChR and to require an alpha4-containing nAChR. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:CHRNB4) increases a(MESH:"Receptors, Nicotinic") View Subject | View Object

On the other hand, neuronal nicotinic receptors are formed by the combination of only two types of subunits (α2-10 and β2-4) PubMed:26813123

Appears in Networks:
Annotations
MeSH
Neurons

p(HGNC:CHRNB4) hasVariant p(HGNC:CHRNB4, var("?")) View Subject | View Object

Appears in Networks:

p(HGNC:CHRNB4) association act(a(CHEBI:nicotine)) View Subject | View Object

Moreover, nAChRs containing β4, α2 and α5 in the habenulo-interpeduncular systems are necessary for nicotine withdrawal in mice107 PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

p(HGNC:CHRNB4) association path(MESH:Craving) View Subject | View Object

β4 deletion abolishes withdrawal signs in the mouse208, and α3 and β4 are also present in the PNS, supporting the view that they might be directly involved in craving and relapse — an area that is largely unexplored in the development of medications to assist with smoking cessation. PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

p(HGNC:CHRNB4) association path(MESH:Recurrence) View Subject | View Object

β4 deletion abolishes withdrawal signs in the mouse208, and α3 and β4 are also present in the PNS, supporting the view that they might be directly involved in craving and relapse — an area that is largely unexplored in the development of medications to assist with smoking cessation. PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

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