ReviewFrontiers in cellular neuroscience2014
The sodium leak channel, NALCN, in health and disease.
Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 171 citations in OpenAlex.
- Article
- Deletion of the sodium leak channel NALCN in dopamine neurons alters D2R-mediated signalling and psychostimulant responsiveness.The Journal of physiology · 2026Article
- The Effects of CaMembranes · 2026Article
- The sodium leak channel NALCN in Drd2Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Reversible high-fat ketogenic formula-induced hypertriglyceridemia in a child with NALCN mutation on a ketogenic diet: a case report.Molecular biology reports · 2026Article
- Cognitive-Enhancing Effects of Bioactive Compounds and Traditional Herbal Medicines in Elderly Patients with Metabolic Syndrome.Biomolecules · 2026Review
- From a Multi-Omics Signature to a Therapeutic Candidate: Computational Prediction and Experimental Validation in Liver Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Progress in the study of ion channel function, mechanisms, and mathematical modeling in Parkinson's disease.iScience · 2026Review
- Tachykinergic signaling mediated by NK1 receptors in the respiratory parafacial region drives respiratory output and contributes to the chemoreflex response to COPflugers Archiv : European journal of physiology · 2026Article
- NALCN/Cch1 channelosome subunits originated in early eukaryotes.The Journal of general physiology · 2025Article
- Stress-induced reduction of sodium leak currents causes social deficits by impairing dorsal dentate gyrus-medial septum glutamatergic projection.Molecular psychiatry · 2025Article
- A New Variant in the NALCN Channel Is Responsible for Cerebellar Ataxia and Cognitive Impairment.Genes · 2025Article
- Article
- The patient-specific mouse model with Foxg1 frameshift mutation provides insights into the pathophysiology of FOXG1 syndrome.Nature communications · 2025Article
- Genetic Architecture of Hock Joint Bumps in Pigs: Insights from ROH and GWAS Analyses.Animals : an open access journal from MDPI · 2025Article
- Article
- Comprehensive genetic screening of 70 severe adolescent idiopathic scoliosis probands reveals novel pathogenic variants and syndromic associations.Frontiers in medicine · 2025Article
- Prenatal black carbon exposure and DNA methylation in umbilical cord blood.International journal of hygiene and environmental health · 2025Article
- NALCN expression is down-regulated and associated with immune infiltration in gastric cancer.Frontiers in immunology · 2025Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ion channels are crucial components of cellular excitability and are involved in many neurological diseases. This review focuses on the sodium leak, G protein-coupled receptors (GPCRs)-activated NALCN channel that is predominantly expressed in neurons where it regulates the resting membrane potential and neuronal excitability. NALCN is part of a complex that includes not only GPCRs, but also UNC-79, UNC-80, NLF-1 and src family of Tyrosine kinases (SFKs). There is growing evidence that the NALCN channelosome critically regulates its ion conduction. Both in mammals and invertebrates, animal models revealed an involvement in many processes such as locomotor behaviors, sensitivity to volatile anesthetics, and respiratory rhythms. There is also evidence that alteration in this NALCN channelosome can cause a wide variety of diseases. Indeed, mutations in the NALCN gene were identified in Infantile Neuroaxonal Dystrophy (INAD) patients, as well as in patients with an Autosomal Recessive Syndrome with severe hypotonia, speech impairment, and cognitive delay. Deletions in NALCN gene were also reported in diseases such as 13q syndrome. In addition, genes encoding NALCN, NLF- 1, UNC-79, and UNC-80 proteins may be susceptibility loci for several diseases including bipolar disorder, schizophrenia, Alzheimer's disease, autism, epilepsy, alcoholism, cardiac diseases and cancer. Although the physiological role of the NALCN channelosome is poorly understood, its involvement in human diseases should foster interest for drug development in the near future. Toward this goal, we review here the current knowledge on the NALCN channelosome in physiology and diseases.
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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.