ArticleNature communications2020
Intellectual disability-associated UNC80 mutations reveal inter-subunit interaction and dendritic function of the NALCN channel complex.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
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- Unveiling the functional and evolutionary landscape of RNA editing in chicken using genomics and transcriptomics.Zoological research · 2022Article
- Cellular and genetic drivers of RNA editing variation in the human brain.Nature communications · 2022Article
- Architecture of the human NALCN channelosome.Cell discovery · 2022Article
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- Case Report: AFrontiers in pediatrics · 2022Article
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- Case Report: Complete Maternal Uniparental Disomy of Chromosome 2 With a NovelFrontiers in genetics · 2021Article
- De Novo Partial 13q22-q34 Trisomy with Typical Neurological and Immunological Findings: A Case Report with New Genetic Insights.Brain sciences · 2020Article
- Structure of the human sodium leak channel NALCN.Nature · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The sodium-leak channel NALCN forms a subthreshold sodium conductance that controls the resting membrane potentials of neurons. The auxiliary subunits of the channel and their functions in mammals are largely unknown. In this study, we demonstrate that two large proteins UNC80 and UNC79 are subunits of the NALCN complex. UNC80 knockout mice are neonatal lethal. The C-terminus of UNC80 contains a domain that interacts with UNC79 and overcomes a soma-retention signal to achieve dendritic localization. UNC80 lacking this domain, as found in human patients, still supports whole-cell NALCN currents but lacks dendritic localization. Our results establish the subunit composition of the NALCN complex, uncover the inter-subunit interaction domains, reveal the functional significance of regulation of dendritic membrane potential by the sodium-leak channel complex, and provide evidence supporting that genetic variations found in individuals with intellectual disability are the causes for the phenotype observed in patients.
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