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- W2000892197 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." @default.
- W2000892197 created "2016-06-24" @default.
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- W2000892197 date "2014-04-01" @default.
- W2000892197 modified "2023-10-10" @default.
- W2000892197 title "NRA-2, a Nicalin Homolog, Regulates Neuronal Death by Controlling Surface Localization of Toxic Caenorhabditis elegans DEG/ENaC Channels" @default.
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- W2000892197 doi "https://doi.org/10.1074/jbc.m113.533695" @default.
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