ArticleThe EMBO journal2005
Identification and characterization of novel nicotinic receptor-associated proteins in Caenorhabditis elegans.
Article in The EMBO journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 187 citations in OpenAlex.
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- The nematode (Ascaris suum) intestine is a location of synergistic anthelmintic effects of Cry5B and levamisole.PLoS pathogens · 2024Article
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- Two residues determine nicotinic acetylcholine receptor requirement for RIC-3.Protein science : a publication of the Protein Society · 2023Article
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- Bioassay-Guided Isolation of Anthelmintic Components fromInternational journal of molecular sciences · 2022Article
- Reconstitution of an N-AChR from Brugia malayi, an evolved change in acetylcholine receptor accessory protein requirements in filarial parasites.PLoS pathogens · 2022Article
- Measuring Caenorhabditis elegans Sensitivity to the Acetylcholine Receptor Agonist Levamisole.Journal of visualized experiments : JoVE · 2022Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nicotinic acetylcholine receptors (nAChRs) mediate fast excitatory neurotransmission in neurons and muscles. To identify nAChR accessory proteins, which may regulate their expression or function, we performed tandem affinity purification of the levamisole-sensitive nAChR from Caenorhabditis elegans, mass spectrometry of associated components, and RNAi-based screening for effects on in vivo nicotine sensitivity. Among the proteins identified was the calcineurin A subunit TAX-6, which appeared to function as a negative regulator of nAChR activity. We also identified five proteins not previously linked to nAChR function, whose inactivation conferred nicotine resistance, implicating them as positive regulators of nAChR activity. Of these, the copine NRA-1 colocalized with the levamisole receptor at neuronal and muscle plasma membranes, and, when mutated, caused reduced synaptic nAChR expression. Loss of SOC-1, which acts in receptor tyrosine kinase (RTK) signaling, also reduced synaptic levamisole receptor levels, as did mutations in the fibroblast growth factor receptor EGL-15, and another RTK, CAM-1. Thus, tandem affinity purification is a viable approach to identify novel proteins regulating neurotransmitter receptor activity or expression in model systems like C. elegans.
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