ArticleThe Journal of biological chemistry2014
NRA-2, a nicalin homolog, regulates neuronal death by controlling surface localization of toxic Caenorhabditis elegans DEG/ENaC channels.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Exploring the molecular composition of the multipass translocon in its native membrane environment.Life science alliance · 2024Article
- Reconstitution of an N-AChR from Brugia malayi, an evolved change in acetylcholine receptor accessory protein requirements in filarial parasites.PLoS pathogens · 2022Article
- The mechanisms of integral membrane protein biogenesis.Nature reviews. Molecular cell biology · 2022Review
- Anthelmintic resistance and homeostatic plasticity (Brugia malayi).Scientific reports · 2021Article
- Identification of the soluble EphA7-interacting protein Nicalin as a regulator of EphA7 expression.Molecular and cellular biochemistry · 2021Article
- Article
- RNAi Screen Identifies Novel Regulators of RNP Granules in the Caenorhabditis elegans Germ Line.G3 (Bethesda, Md.) · 2016Article
- Metabolome and proteome changes with aging in Caenorhabditis elegans.Experimental gerontology · 2015Article
- Subunit composition of a DEG/ENaC mechanosensory channel of Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperactivated DEG/ENaCs induce neuronal death through excessive cation influx and disruption of intracellular calcium homeostasis. Caenorhabditis elegans DEG/ENaC MEC-4 is hyperactivated by the (d) mutation and induces death of touch neurons. The analogous substitution in MEC-10 (MEC-10(d)) co-expressed in the same neurons is only mildly neurotoxic. We exploited the lower toxicity of MEC-10(d) to identify RNAi knockdowns that enhance neuronal death. We report here that knock-out of the C. elegans nicalin homolog NRA-2 enhances MEC-10(d)-induced neuronal death. Cell biological assays in C. elegans neurons show that NRA-2 controls the distribution of MEC-10(d) between the endoplasmic reticulum and the cell surface. Electrophysiological experiments in Xenopus oocytes support this notion and suggest that control of channel distribution by NRA-2 is dependent on the subunit composition. We propose that nicalin/NRA-2 functions in a quality control mechanism to retain mutant channels in the endoplasmic reticulum, influencing the extent of neuronal death. Mammalian nicalin may have a similar role in DEG/ENaC biology, therefore influencing pathological conditions like ischemia.
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