Baylis, H.A., Matsuda, K., Squire, M.D., Fleming, J.T., Harvey, R.J., Darlison, M.G., Barnard, E.A. and Sattelle, D.B. (1997) ACR-3, a Caenorhabditis elegans nicotinic acetylcholine receptor subunit. Molecular cloning and functional expression. Receptors & Channels, 5 (3-4). pp. 149-158.
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The molecular cloning and functional co-expression of a novel nicotinic acetylcholine receptor (nAChR) non-alpha subunit gene, acr-3, is described. Previously we determined the sequence and demonstrated the functional co-expression of acr-2, a nAChR non-alpha subunit gene from Caenorhabditis elegans. Analysis of the acr-2 genomic DNA revealed the existence of another potential nAChR subunit gene, acr-3, in the same orientation, only 281 bp downstream of acr-2. A cDNA containing the entire acr-3 coding sequence was isolated by RT-PCR and sequenced. The predicted protein contains the conserved features typical of nAChR non-alpha subunits and most closely resembles other invertebrate nAChR non-alpha polypeptides. Unusually, the highly conserved glycine residue (equivalent to residue 240 in the Torpedo alpha subunit) upstream of transmembrane domain 2 (m2) is replaced by a serine residue in ACR-3. When acr-3 cDNA was injected alone into Xenopus oocytes no levamisole-gated channel activity was observed. However when co-expressed with a C. elegans alpha subunit (UNC-38), ACR-3 contributed to the formation of levamisole-gated channels. The response of this hetero-oligomer to levamisole (100 microM) was reduced by the nAChR antagonists mecamylamine (1 microM) and d-tubocurarine (10 microM).
|Departments, units and centres:||Department of Pharmacology > Department of Pharmacology|
|Journal or Publication Title:||Receptors & Channels|
|Deposited By:||Library Staff|
|Deposited On:||01 Apr 2011 12:49|
|Last Modified:||16 Jun 2011 11:12|
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