NAV1.5 Voltage-Gated Sodium Channel
"NAV1.5 Voltage-Gated Sodium Channel" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of CARDIOMYOCYTES. Defects in the SCN5A gene, which codes for the alpha subunit of this sodium channel, are associated with a variety of CARDIAC DISEASES that result from loss of sodium channel function.
Descriptor ID |
D062554
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MeSH Number(s) |
D12.776.157.530.400.875.750.500 D12.776.543.550.450.875.750.500 D12.776.543.585.400.875.750.500 D12.776.631.960.500
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Concept/Terms |
NAV1.5 Voltage-Gated Sodium Channel- NAV1.5 Voltage-Gated Sodium Channel
- NAV1.5 Voltage Gated Sodium Channel
- Voltage-Gated Sodium Channel Type 5
- Voltage Gated Sodium Channel Type 5
- Type 5 Voltage-Gated Sodium Channel
- Type 5 Voltage Gated Sodium Channel
Voltage-Gated Sodium Channel Type 5 Subunit alpha- Voltage-Gated Sodium Channel Type 5 Subunit alpha
- Voltage Gated Sodium Channel Type 5 Subunit alpha
- SCN5A Sodium Channel alpha Subunit
- Voltage-Gated Na+ Channel Na(v)1.5a
- Sodium Channel Protein Type 5 Subunit alpha
- Sodium Channel, Voltage-Gated, Type V, alpha Subunit
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Below are MeSH descriptors whose meaning is more general than "NAV1.5 Voltage-Gated Sodium Channel".
Below are MeSH descriptors whose meaning is more specific than "NAV1.5 Voltage-Gated Sodium Channel".
This graph shows the total number of publications written about "NAV1.5 Voltage-Gated Sodium Channel" by people in this website by year, and whether "NAV1.5 Voltage-Gated Sodium Channel" was a major or minor topic of these publications.
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Year | Major Topic | Minor Topic | Total |
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2008 | 0 | 1 | 1 |
2009 | 0 | 1 | 1 |
2014 | 1 | 0 | 1 |
2017 | 0 | 1 | 1 |
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Below are the most recent publications written about "NAV1.5 Voltage-Gated Sodium Channel" by people in Profiles.
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Finet JE, Wan X, Donahue JK. Fusion of Anthopleurin-B to AAV2 increases specificity of cardiac gene transfer. Virology. 2018 01 01; 513:43-51.
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Magnani JW, Brody JA, Prins BP, Arking DE, Lin H, Yin X, Liu CT, Morrison AC, Zhang F, Spector TD, Alonso A, Bis JC, Heckbert SR, Lumley T, Sitlani CM, Cupples LA, Lubitz SA, Soliman EZ, Pulit SL, Newton-Cheh C, O'Donnell CJ, Ellinor PT, Benjamin EJ, Muzny DM, Gibbs RA, Santibanez J, Taylor HA, Rotter JI, Lange LA, Psaty BM, Jackson R, Rich SS, Boerwinkle E, Jamshidi Y, Sotoodehnia N. Sequencing of SCN5A identifies rare and common variants associated with cardiac conduction: Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Circ Cardiovasc Genet. 2014 Jun; 7(3):365-73.
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Cheng J, Van Norstrand DW, Medeiros-Domingo A, Valdivia C, Tan BH, Ye B, Kroboth S, Vatta M, Tester DJ, January CT, Makielski JC, Ackerman MJ. Alpha1-syntrophin mutations identified in sudden infant death syndrome cause an increase in late cardiac sodium current. Circ Arrhythm Electrophysiol. 2009 Dec; 2(6):667-76.
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Van Norstrand DW, Tester DJ, Ackerman MJ. Overrepresentation of the proarrhythmic, sudden death predisposing sodium channel polymorphism S1103Y in a population-based cohort of African-American sudden infant death syndrome. Heart Rhythm. 2008 May; 5(5):712-5.
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Mohler PJ, Rivolta I, Napolitano C, LeMaillet G, Lambert S, Priori SG, Bennett V. Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the surface of cardiomyocytes. Proc Natl Acad Sci U S A. 2004 Dec 14; 101(50):17533-8.