ArticleScience advances2020
The NALCN channel complex is voltage sensitive and directly modulated by extracellular calcium.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 79 citations in OpenAlex.
- Tunable AMPA receptor function via recurrent evolution of heterotetramers.The Journal of general physiology · 2026Article
- The Effects of CaMembranes · 2026Article
- Divalent cation depletion enhances intrinsic neuronal excitability through CaSR-dependent modulation of threshold ion channels.PNAS nexus · 2026Article
- Comparative Ion Channel Transcriptomes of NK1R and Somatostatin Neurons in the PreBötzinger Complex of the Ventrolateral Medulla.Molecular neurobiology · 2026Article
- Comparative Ion Channel Transcriptomes of NK1R and Somatostatin Neurons in the preBötzinger Complex of the Ventrolateral Medulla.Research square · 2026Article
- Identification of Growth-Related SNPs and Genes Through Genome-Wide Association Studies in Pseudobagrus ussuriensis.Marine biotechnology (New York, N.Y.) · 2026Article
- NaThe Journal of membrane biology · 2026Article
- Cell-intrinsic mechanisms underlying spontaneous activity in the mouse visual cortical slice: implications for fragile X pathophysiology.Journal of neurophysiology · 2026Article
- NALCN/Cch1 channelosome subunits originated in early eukaryotes.The Journal of general physiology · 2025Article
- Genome-Wide Association Study of Plasma Sodium Concentrations with and without Exposure to Thiazide Diuretics.Journal of the American Society of Nephrology : JASN · 2025Article
- Article
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- NALCN expression is down-regulated and associated with immune infiltration in gastric cancer.Frontiers in immunology · 2025Article
- The background sodium leak channel NALCN is a major controlling factor in pituitary cell excitability.The Journal of physiology · 2025Article
- Evaluation of mechanisms involved in regulation of intrinsic excitability by extracellular calcium in CA1 pyramidal neurons of rat.Journal of neurochemistry · 2025Article
- In vivo dynamic tracking of cerebral chloride regulation using molecularly tailored liquid/liquid interfacial ultramicro iontronics.Science advances · 2024Article
- Article
- Identification of the modulatory CaOpen biology · 2024Article
- Unplugging lateral fenestrations of NALCN reveals a hidden drug binding site within the pore region.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The NaeLife · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sodium leak channel (NALCN) is essential for survival in mammals: NALCN mutations are life-threatening in humans and knockout is lethal in mice. However, the basic functional and pharmacological properties of NALCN have remained elusive. Here, we found that robust function of NALCN in heterologous systems requires co-expression of UNC79, UNC80, and FAM155A. The resulting NALCN channel complex is constitutively active and conducts monovalent cations but is blocked by physiological concentrations of extracellular divalent cations. Our data support the notion that NALCN is directly responsible for the increased excitability observed in a variety of neurons in reduced extracellular Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.