Neuronal acetylcholine receptor subunit alpha-7, also known as nAChRα7, is a protein that in humans is encoded by the CHRNA7 gene.[5] The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR).

CHRNA7
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesCHRNA7, CHRNA7-2, NACHRA7, cholinergic receptor nicotinic alpha 7 subunit
External IDsOMIM: 118511; MGI: 99779; HomoloGene: 593; GeneCards: CHRNA7; OMA:CHRNA7 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_000746
NM_001190455

NM_007390

RefSeq (protein)

NP_000737
NP_001177384

NP_031416

Location (UCSC)Chr 15: 31.92 – 32.17 MbChr 7: 62.75 – 62.86 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

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The nicotinic acetylcholine receptors (nAChRs) are members of a superfamily of ligand-gated ion channels that mediate fast signal transmission at synapses. The nAChRs are thought to be hetero-pentamers composed of homologous subunits. The proposed structure for each subunit is a conserved N-terminal extracellular domain followed by three conserved transmembrane domains, a variable cytoplasmic loop, a fourth conserved transmembrane domain, and a short C-terminal extracellular region. The protein encoded by this gene forms a homo-oligomeric channel, displays marked permeability to calcium ions and is a major component of brain nicotinic receptors that are blocked by, and highly sensitive to, alpha-bungarotoxin. Once this receptor binds acetylcholine, it undergoes an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. This gene is located in a region identified as a major susceptibility locus for juvenile myoclonic epilepsy and a chromosomal location involved in the genetic transmission of schizophrenia. An evolutionarily recent partial duplication event in this region results in a hybrid containing sequence from this gene and a novel FAM7A gene.[6]

Disruption of alpha-7 nicotinic receptors in schizophrenia is believed to contribute at least in part to the abnormally high prevalence of extremely heavy smoking in those affected by the disease. This observed particularly high nicotine intake compared to the average smoker is hypothesized to be a subconscious effort to activate the low-affinity alpha-7 receptors.

Interactions

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CHRNA7 has been shown to interact with FYN.[7]

Gene expression

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The CHRNA7 gene is primarily expressed in the posterior amygdalar nucleus and the field CA3 of Ammon's horn in the mouse, and in the mammillary body in humans. Gene expression patterns from the Allen Brain Atlases can be seen here.

See also

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References

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  1. ^ a b c ENSG00000175344, ENSG00000282088 GRCh38: Ensembl release 89: ENSG00000274542, ENSG00000175344, ENSG00000282088Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000030525Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Chini B, Raimond E, Elgoyhen AB, Moralli D, Balzaretti M, Heinemann S (Jun 1994). "Molecular cloning and chromosomal localization of the human alpha 7-nicotinic receptor subunit gene (CHRNA7)". Genomics. 19 (2): 379–381. doi:10.1006/geno.1994.1075. PMID 8188270.
  6. ^ "Entrez Gene: CHRNA7 cholinergic receptor, nicotinic, alpha 7".
  7. ^ Kihara T, Shimohama S, Sawada H, Honda K, Nakamizo T, Shibasaki H, Kume T, Akaike A (April 2001). "alpha 7 nicotinic receptor transduces signals to phosphatidylinositol 3-kinase to block A beta-amyloid-induced neurotoxicity". J. Biol. Chem. 276 (17): 13541–13546. doi:10.1074/jbc.M008035200. PMID 11278378.

Further reading

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This article incorporates text from the United States National Library of Medicine, which is in the public domain.