ReviewFrontiers in pharmacology2015
Physiological and Pathophysiological Insights of Nav1.4 and Nav1.5 Comparison.
Review in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Gene variant effects across sodium channelopathies predict function and guide precision therapy.Brain : a journal of neurology · 2022Pooled it
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- Association between voltage-gated sodium channel gene polymorphisms and chronic oxaliplatin-induced peripheral neuropathy in Japanese patients with colorectal cancer.Journal of pharmaceutical health care and sciences · 2026Article
- Osteoarthritis: molecular pathogenesis and potential therapeutic options.Signal transduction and targeted therapy · 2026Review
- Article
- Isoform-specific N-linked glycosylation of NaV channel α-subunits alters β-subunit binding sites.The Journal of general physiology · 2025Article
- Biophysical mechanisms of myocardium sodium channelopathies.Pflugers Archiv : European journal of physiology · 2024Review
- Skeletal muscle differentiation induces wide-ranging nucleosome repositioning in muscle gene promoters.Scientific reports · 2024Article
- Novel compound heterozygous mutations inHeliyon · 2024Article
- Current state of the epilepsy drug and device pipeline.Epilepsia · 2024Review
- Nernst-Planck-Gaussian finite element modelling of CaFrontiers in physiology · 2024Article
- Functional effects of drugs and toxins interacting with NaFrontiers in pharmacology · 2024Review
- Molecular and Cellular Mechanisms of Action of Cannabidiol.Molecules (Basel, Switzerland) · 2023Review
- Synthesis, Pharmacological Evaluation, and Molecular Modeling of Lappaconitine-1,5-Benzodiazepine Hybrids.Molecules (Basel, Switzerland) · 2023Article
- Article
- Closed-state inactivation of cardiac, skeletal, and neuronal sodium channels is isoform specific.The Journal of general physiology · 2022Article
- Spliced isoforms of the cardiac Nav1.5 channel modify channel activation by distinct structural mechanisms.The Journal of general physiology · 2022Article
- Evidence that toxin resistance in poison birds and frogs is not rooted in sodium channel mutations and may rely on "toxin sponge" proteins.The Journal of general physiology · 2021Article
- Cannabidiol Selectively Binds to the Voltage-Gated Sodium Channel NaBiomedicines · 2021Article
- Finite element analysis predicts CaScientific reports · 2021Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in Nav1.4 and Nav1.5 α-subunits have been associated with muscular and cardiac channelopathies, respectively. Despite intense research on the structure and function of these channels, a lot of information is still missing to delineate the various physiological and pathophysiological processes underlying their activity at the molecular level. Nav1.4 and Nav1.5 sequences are similar, suggesting structural and functional homologies between the two orthologous channels. This also suggests that any characteristics described for one channel subunit may shed light on the properties of the counterpart channel subunit. In this review article, after a brief clinical description of the muscular and cardiac channelopathies related to Nav1.4 and Nav1.5 mutations, respectively, we compare the knowledge accumulated in different aspects of the expression and function of Nav1.4 and Nav1.5 α-subunits: the regulation of the two encoding genes (SCN4A and SCN5A), the associated/regulatory proteins and at last, the functional effect of the same missense mutations detected in Nav1.4 and Nav1.5. First, it appears that more is known on Nav1.5 expression and accessory proteins. Because of the high homologies of Nav1.5 binding sites and equivalent Nav1.4 sites, Nav1.5-related results may guide future investigations on Nav1.4. Second, the analysis of the same missense mutations in Nav1.4 and Nav1.5 revealed intriguing similarities regarding their effects on membrane excitability and alteration in channel biophysics. We believe that such comparison may bring new cues to the physiopathology of cardiac and muscular 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.