CHRNA7

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. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2012]

Full Name

Cholinergic Receptor Nicotinic Alpha 7 Subunit

Function

After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. The channel is blocked by alpha-bungarotoxin.

Biological Process

Acetylcholine receptor signaling pathway Source: ARUK-UCL
Activation of MAPK activity Source: UniProtKB
Calcium ion transport Source: UniProtKB
Cellular calcium ion homeostasis Source: UniProtKB
Chemical synaptic transmission Source: GO_Central
Cognition Source: UniProtKB
Dendrite arborization Source: ARUK-UCL
Dendritic spine organization Source: ARUK-UCL
Ion transmembrane transport Source: ParkinsonsUK-UCL
Ion transport Source: UniProtKB
Learning or memory Source: ARUK-UCL
Memory Source: ARUK-UCL
Modulation of excitatory postsynaptic potential Source: ARUK-UCL
Negative regulation of amyloid-beta formation Source: ARUK-UCL
Negative regulation of tumor necrosis factor production Source: MGI
Nervous system process Source: GO_Central
Positive regulation of amyloid-beta formation Source: ARUK-UCL
Positive regulation of angiogenesis Source: UniProtKB
Positive regulation of cell population proliferation Source: UniProtKB
Positive regulation of CoA-transferase activity Source: ARUK-UCL
Positive regulation of ERK1 and ERK2 cascade Source: ARUK-UCL
Positive regulation of excitatory postsynaptic potential Source: ARUK-UCL
Positive regulation of long-term synaptic potentiation Source: ARUK-UCL
Positive regulation of protein metabolic process Source: ARUK-UCL
Positive regulation of protein phosphorylation Source: ARUK-UCL
Regulation of amyloid fibril formation Source: ARUK-UCL
Regulation of amyloid precursor protein catabolic process Source: ARUK-UCL
Regulation of membrane potential Source: GO_Central
Regulation of neuron death Source: ARUK-UCL
Response to acetylcholine Source: ARUK-UCL
Response to amyloid-beta Source: ARUK-UCL
Response to hypoxia Source: UniProtKB
Response to nicotine Source: UniProtKB
Sensory processing Source: ARUK-UCL
Short-term memory Source: ARUK-UCL
Signal transduction Source: UniProtKB
Synapse organization Source: ARUK-UCL
Synaptic transmission, cholinergic Source: GO_Central

Cellular Location

Postsynaptic cell membrane; Cell membrane. TMEM35A/NACHO promotes its trafficking to the cell membrane (PubMed:27789755). RIC3 promotes its trafficking to the cell membrane (By similarity).

Topology

Extracellular: 23-230
Helical: 231-255
Helical: 262-280
Helical: 296-317
Cytoplasmic: 318-469
Helical: 470-490

PTM

Glycosylations at Asn-46, Asn-90 and Asn-133 are essential for TMEM35A/NACHO-mediated proper subunit assembly and trafficking to the cell membrane.