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Entity

Name
alpha-4-containing nAChR
Namespace
HBP
Namespace Version
20181221
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/bd0996a28201cad363557315043c6392e31abf58/export/hbp-names.belns

Appears in Networks 4

In-Edges 9

path(MESH:"Drug Tolerance") association a(HBP:"alpha-4-containing nAChR") 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

a(CHEBI:nicotine) causesNoChange a(HBP:"alpha-4-containing nAChR") View Subject | View Object

While chronic nicotine does not change the abundance or function of alpha4* nAChRs in the somata of substantia nigra pars compacta dopaminergic neurons, it does suppress baseline firing rates of these DA neurons. PubMed:21482353

a(CHEBI:nicotine) increases act(a(HBP:"alpha-4-containing nAChR")) View Subject | View Object

These contrasting effects on GABA and DA neurons are due to upregulated alpha4* nAChR responses in GABA neurons, at both somata and synaptic terminals PubMed:21482353

a(CHEBI:nicotine) increases act(a(HBP:"alpha-4-containing nAChR")) View Subject | View Object

Chronic nicotine upregulates alpha4* nAChRs in dopaminergic presynaptic terminals, apparently leading to increased resting dopamine release from those terminals PubMed:21482353

a(CHEBI:nicotine) increases tloc(a(HBP:"alpha-4-containing nAChR"), fromLoc(GO:"endoplasmic reticulum"), toLoc(GO:"extracellular region")) View Subject | View Object

The chaperoning of nAChRs by nicotine enhances the export of alpha4beta2 nAChRs from the endoplasmic reticulum (ER), and this leads to a general increase in ER exit sites (Srinivasan et al., 2011) PubMed:21482353

bp(GO:aging) negativeCorrelation a(HBP:"alpha-4-containing nAChR") View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

path(MESH:"Alzheimer Disease") negativeCorrelation a(HBP:"alpha-4-containing nAChR") View Subject | View Object

A decrease in protein levels of the alpha4 nAChR but not of the alpha3 and alpha7 nAChRs was reported by Martin-Ruiz et al (1999) PubMed:11230871

path(MESH:Schizophrenia) causesNoChange a(HBP:"alpha-4-containing nAChR") View Subject | View Object

Interestingly, a reduction in the protein level of alpha7 has also been measured in the frontal cortex of patients with schizophrenia (Guan et al 1999), whereas no decrease was measured in the alpha4 nAChR protein level (Guan et al 1999) PubMed:11230871

Out-Edges 3

a(HBP:"alpha-4-containing nAChR") 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

a(HBP:"alpha-4-containing nAChR") negativeCorrelation bp(GO:aging) View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

a(HBP:"alpha-4-containing nAChR") negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

A decrease in protein levels of the alpha4 nAChR but not of the alpha3 and alpha7 nAChRs was reported by Martin-Ruiz et al (1999) PubMed:11230871

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.