| Literature DB >> 11867529 |
Sarah Halevi1, Jim McKay, Mark Palfreyman, Lina Yassin, Margalit Eshel, Erik Jorgensen, Millet Treinin.
Abstract
Mutations in ric-3 (resistant to inhibitors of cholinesterase) suppress the neuronal degenerations caused by a gain of function mutation in the Caenorhabditis elegans DEG-3 acetylcholine receptor. RIC-3 is a novel protein with two transmembrane domains and extensive coiled-coil domains. It is expressed in both muscles and neurons, and the protein is concentrated within the cell bodies. We demonstrate that RIC-3 is required for the function of at least four nicotinic acetylcholine receptors. However, GABA and glutamate receptors expressed in the same cells are unaffected. In ric-3 mutants, the DEG-3 receptor accumulates in the cell body instead of in the cell processes. Moreover, co-expression of ric-3 in Xenopus laevis oocytes enhances the activity of the C.elegans DEG-3/DES-2 and of the rat alpha-7 acetylcholine receptors. Together, these data suggest that RIC-3 is specifically required for the maturation of acetylcholine receptors.Entities:
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Year: 2002 PMID: 11867529 PMCID: PMC125878 DOI: 10.1093/emboj/21.5.1012
Source DB: PubMed Journal: EMBO J ISSN: 0261-4189 Impact factor: 11.598