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.
To see the data from this visualization as text, click here.
Year | Major Topic | Minor Topic | Total |
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2004 | 0 | 1 | 1 | 2011 | 0 | 1 | 1 | 2014 | 3 | 0 | 3 | 2017 | 2 | 0 | 2 |
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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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Sanner K, Mueller-Leisse J, Zormpas C, Duncker D, Leffler A, Veltmann C. A Novel SCN5A Variant Causes Temperature-Sensitive Loss Of Function in a Family with Symptomatic Brugada Syndrome, Cardiac Conduction Disease, and Sick Sinus Syndrome. Cardiology. 2021; 146(6):754-762.
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Peters CH, Watkins AR, Poirier OL, Ruben PC. E1784K, the most common Brugada syndrome and long-QT syndrome type 3 mutant, disrupts sodium channel inactivation through two separate mechanisms. J Gen Physiol. 2020 09 07; 152(9).
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Zhang J, Vincent KP, Peter AK, Klos M, Cheng H, Huang SM, Towne JK, Ferng D, Gu Y, Dalton ND, Chan Y, Li R, Peterson KL, Chen J, McCulloch AD, Knowlton KU, Ross RS. Cardiomyocyte Expression of ZO-1 Is Essential for Normal Atrioventricular Conduction but Does Not Alter Ventricular Function. Circ Res. 2020 07 03; 127(2):284-297.
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Hooker JM, Strebl MG, Schroeder FA, Wey HY, Ambardekar AV, McKinsey TA, Schoenberger M. Imaging cardiac SCN5A using the novel F-18 radiotracer radiocaine. Sci Rep. 2017 02 16; 7:42136.
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Te Riele AS, Agullo-Pascual E, James CA, Leo-Macias A, Cerrone M, Zhang M, Lin X, Lin B, Sobreira NL, Amat-Alarcon N, Marsman RF, Murray B, Tichnell C, van der Heijden JF, Dooijes D, van Veen TA, Tandri H, Fowler SJ, Hauer RN, Tomaselli G, van den Berg MP, Taylor MR, Brun F, Sinagra G, Wilde AA, Mestroni L, Bezzina CR, Calkins H, Peter van Tintelen J, Bu L, Delmar M, Judge DP. Multilevel analyses of SCN5A mutations in arrhythmogenic right ventricular dysplasia/cardiomyopathy suggest non-canonical mechanisms for disease pathogenesis. Cardiovasc Res. 2017 01; 113(1):102-111.
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Clendenen N, Cannon AD, Porter S, Robards CB, Parker AS, Clendenen SR. Whole-exome sequencing of a family with local anesthetic resistance. Minerva Anestesiol. 2016 10; 82(10):1089-1097.
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Shi D, Xie D, Zhang H, Zhao H, Huang J, Li C, Liu Y, Lv F, The E, Liu Y, Yuan T, Wang S, Chen J, Pan L, Yu Z, Liang D, Zhu W, Zhang Y, Li L, Peng L, Li J, Chen YH. Reduction in dynamin-2 is implicated in ischaemic cardiac arrhythmias. J Cell Mol Med. 2014 Oct; 18(10):1992-9.
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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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Frenz CT, Hansen A, Dupuis ND, Shultz N, Levinson SR, Finger TE, Dionne VE. NaV1.5 sodium channel window currents contribute to spontaneous firing in olfactory sensory neurons. J Neurophysiol. 2014 Sep 01; 112(5):1091-104.
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Takahashi K, Shimizu W, Miyake A, Nabeshima T, Nakayashiro M, Ganaha H. High prevalence of the SCN5A E1784K mutation in school children with long QT syndrome living on the Okinawa islands. Circ J. 2014; 78(8):1974-9.
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