Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Electronic Gene Ontology annotations created by ARBA machine learning models
Stoichiometry of human recombinant neuronal nicotinic receptors containing the b3 subunit expressed in Xenopus oocytes.
-
Human receptor reporter mutations in Xenopus support a 2alpha3:2beta4:1beta3 composition for the tested triplet, contrasted with 2alpha3:3beta4 pair receptors.
"suggesting that the 'triplet' receptor contains one copy of beta3 and two copies each of alpha3 and beta4."
Characterization of the human beta4 nAChR gene and polymorphisms in CHRNA3 and CHRNB4.
Alpha-5/alpha-3 nicotinic receptor subunit alleles increase risk for heavy smoking.
Low ethanol concentration alters CHRNA5 RNA levels during early human development.
Acetylcholine receptor (AChR) α5 subunit variant associated with risk for nicotine dependence and lung cancer reduces (α4β2)₂α5 AChR function.
Nicotine decreases food intake through activation of POMC neurons.
UBXN2A regulates nicotinic receptor degradation by modulating the E3 ligase activity of CHIP.
UBXD4, a UBX-containing protein, regulates the cell surface number and stability of alpha3-containing nicotinic acetylcholine receptors.
Functional interaction between Lypd6 and nicotinic acetylcholine receptors.
Agonist Selectivity and Ion Permeation in the α3β4 Ganglionic Nicotinic Receptor.
-
Human alpha3beta4 receptor structures resolve the principal alpha3 and complementary beta4 binding faces and a 2alpha3:3beta4 assembly under the tested expression conditions.
"pentamers containing two α3 and three β4 subunits"
CAKUT and Autonomic Dysfunction Caused by Acetylcholine Receptor Mutations.
Comparative structure of human neuronal alpha 2-alpha 7 and beta 2-beta 4 nicotinic acetylcholine receptor subunits and functional expression of the alpha 2, alpha 3, alpha 4, alpha 7, beta 2, and beta 4 subunits.
Activation of highly sodium permeable postsynaptic nicotinic acetylcholine receptors
Activation of highly calcium permeable nicotinic acetylcholine receptors
Binding of acetylcholine to highly sodium permeable postsynaptic acetylcholine receptors
Activation of highly calcium permeable postsynaptic nicotinic acetylcholine receptors
Binding of acetylcholine to highly calcium permeable postsynaptic nicotinic acetylcholine receptors
Binding of acetylcholine to highly calcium permeable acetylcholine receptors
Megacystis, mydriasis, and ion channel defect in mice lacking the alpha3 neuronal nicotinic acetylcholine receptor.
-
Mouse alpha3 loss severely reduces ganglionic ACh-activated currents and autonomic function while bladder contraction to electrical stimulation or carbamoylcholine persists.
"Bladder strips from -/- mice failed to contract in response to 0.1 mM nicotine, but did contract in response to electrical field stimulation or carbamoylcholine."
Mice lacking specific nicotinic acetylcholine receptor subunits exhibit dramatically altered spontaneous activity patterns and reveal a limited role for retinal waves in forming ON and OFF circuits in the inner retina.
Nicotinic acetylcholine receptor subtypes in rat superior cervical ganglion neurons as studied by sequential application of two alpha-subunit-specific antibodies.
Methyllycaconitine is a potent antagonist of alpha-conotoxin-MII-sensitive presynaptic nicotinic acetylcholine receptors in rat striatum.
The alpha3 and beta4 nicotinic acetylcholine receptor subunits are necessary for nicotine-induced seizures and hypolocomotion in mice.
A null mutation for the alpha3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner.
The α7 nicotinic acetylcholine receptor function in hippocampal neurons is regulated by the lipid composition of the plasma membrane.