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1. Full Text Biology of cardiac sodium channel Na v1.5 expression
by Rook, Martin B and Evers, Melvin M and Vos, Marc A and Bierhuizen, Marti F.A
Cardiovascular Research, ISSN 0008-6363, 01/2012, Volume 93, Issue 1, pp. 12 - 23
1.5 | Regulation | SCN5A | Cardiac sodium channel | Trafficking
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2. Full Text Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the of cardiomyocytes
by Mohler, Peter J and Rivolta, Ilaria and Napolitano, Carlo and LeMaillet, Guy and Lambert, Stephen and Priori, Silvia G and Bennett, Vann
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2004, Volume 101, Issue 50, pp. 17533 - 17538
SCN5A | Arrhythmia | Targeting | Sudden cardiac death | Trafficking
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3. Full Text Clinical Aspects of Type 3 Long-QT Syndrome: An International Multicenter Study
by Wilde, Arthur A. M and Moss, Arthur J and Kaufman, Elizabeth S and Shimizu, Wataru and Peterson, Derick R and Benhorin, Jesaia and Lopes, Coeli and Towbin, Jeffrey A and Spazzolini, Carla and Crotti, Lia and Zareba, Wojciech and Goldenberg, Ilan and Kanters, Jørgen K and Robinson, Jennifer L and Qi, Ming and Hofman, Nynke and Tester, David J and Bezzina, Connie R and Alders, Marielle and Aiba, Takeshi and Kamakura, Shiro and Miyamoto, Yoshihiro and Anews, Mark L and McNitt, Scott and Polonsky, Bronislava and Schwartz, Peter J and Ackerman, Michael J
Circulation, ISSN 0009-7322, 2016, Volume 134, Issue 12, pp. 872 - 882
Risk stratification in patients with type 3 long-QT syndrome (LQT3) by clinical and genetic characteristics and effectiveness of β-blocker therapy has not been... 
risk assessment | death | arrhythmia | genetic testing | sudden | SCN5A protein | human | long-QT syndrome | cardiac | CARDIAC & CARDIOVASCULAR SYSTEMS | FLECAINIDE | arrhythmia, cardiac | GENOTYPE | PHENOTYPE | SODIUM-CHANNEL | death, sudden, cardiac | THERAPY | IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR | GENE | MUTATION | PERIPHERAL VASCULAR DISEASE | SCN5A protein, human | SCN5A | BETA-BLOCKERS | Syncope - complications | Risk Assessment | Humans | Child, Preschool | Infant | Male | Sex Characteristics | Young Adult | Heart Arrest - drug therapy | Long QT Syndrome - diagnosis | Adolescent | Heart Arrest - etiology | Adult | Female | Registries | Sodium Channels - genetics | Syncope - drug therapy | Long QT Syndrome - drug therapy | Cardiac Conduction System Disease | Child | Electrocardiography - methods | Adrenergic beta-Antagonists - therapeutic use | Treatment outcome | Usage | Analysis | Long QT syndrome | Genetic aspects | Dosage and administration | Adrenergic beta blockers | Risk factors | Genetic screening | Index Medicus | Abridged Index Medicus | risk stratification | sudden cardiac death | long QT syndrome
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4. Full Text Functional dominant-negative mutation of sodium channel subunit gene SCN3B associated with atrial fibrillation in a Chinese GeneID population
by Wang, Pengyun and Wang, Chuchu and Wang, Qing K and Yang, Yanzong and Yang, Bo and Yang, Qinbo and Wu, Gang and Wu, Xiaofen and Shi, Lisong and Xia, Yunlong and Zhang, Rongfeng and Xu, Chengqi and Cheng, Xiang and Li, Sisi and Zhao, Yuanyuan and Fu, Fenfen and Liao, Yuhua and Fang, Fang and Chen, Qiuyun and Tu, Xin
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 07/2010, Volume 398, Issue 1, pp. 98 - 104
► Identification of sodium channel β3 subunit gene SCN3B as a new gene responsible for atrial fibrillation, which is the most common cardiac rhythm disturbance... 
Cardiac sodium current | Mutation | Ion channel | Sodium channel β subunit SCN3B | Atrial fibrillation | Cardiac sodium channel α subunit SCN5A (Nav1.5) | Cardiac sodium channel α subunit SCN5A (Na | 1.5 | OF-FUNCTION MUTATION | SCN5A MUTATION | N1325S | VENTRICULAR-FIBRILLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MECHANISMS | DEATH | IDENTIFICATION | Cardiac sodium channel alpha subunit SCN5A (Na(v)1.5) | Sodium channel beta subunit SCN3B | NA(V)1.5 | BIOPHYSICS | LEADS | BETA-3 SUBUNIT | Cell Line | Humans | Middle Aged | Asian Continental Ancestry Group - genetics | Male | Atrial Fibrillation - genetics | Voltage-Gated Sodium Channel beta-3 Subunit | DNA Mutational Analysis | Base Sequence | Female | Aged | Sodium Channels - genetics | Heart failure | Medical colleges | Tachycardia | Anopheles | Genetic research | Genetic aspects | Cardiology | Coronary heart disease | Index Medicus
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5. Full Text Lamin A mutation impairs interaction with nucleoporin NUP155 and disrupts nucleocytoplasmic transport in atrial fibrillation
by Han, Meng and Zhao, Miao and Cheng, Chen and Huang, Yuan and Han, Shengna and Li, Wenjuan and Tu, Xin and Luo, Xuan and Yu, Xiaoling and Liu, Yinan and Chen, Qiuyun and Ren, Xiang and Wang, Qing Kenneth and Ke, Tie
Human Mutation, ISSN 1059-7794, 03/2019, Volume 40, Issue 3, pp. 310 - 325
Atrial fibrillation (AF) is the most common cardiac arrhythmia. Here, we show the identification and functional characterization of one AF‐associated mutation... 
atrial fibrillation (AF) | mutation | NUP155 | SCN5A/Nav1.5 | LMNA | SHOCK PROTEINS | B-CRYSTALLIN | NUCLEAR-PROTEIN IMPORT | A/C GENE | DILATED CARDIOMYOPATHY | LMNA MUTATIONS | SCN5A VARIANTS | RARE VARIANTS | GENETICS & HEREDITY | DREIFUSS MUSCULAR-DYSTROPHY | NONSENSE MUTATION | Heart | Heat shock proteins | Genetic aspects | RNA | Atrial fibrillation | Porins | Cardiac arrhythmia | Fibrillation | Immunoprecipitation | Arrhythmia | Sodium channels (voltage-gated) | mRNA | Hsp70 protein | Mutation | Protein transport | Cell surface | Nuclear transport | Nav1.5 | SCN5A
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6. Full Text Brugada syndrome disease phenotype explained in apparently benign sodium channel mutations
by Hoshi, Malcolm and Du, Xi X and Shinlapawittayatorn, Krekwit and Liu, Haiyan and Chai, Sam and Wan, Xiaoping and Ficker, Eckhard and Deschênes, Isabelle
Circulation: Cardiovascular Genetics, ISSN 1942-325X, 2014, Volume 7, Issue 2, pp. 123 - 131
Background- Brugada syndrome (BrS) is an arrhythmogenic disorder that has been linked to mutations in SCN5A, the gene encoding for the pore-forming... 
Human | Brugada syndrome | Cardiac | Electrophysiology | Ion channels | SCN5A protein | Arrhythmias | CARDIAC & CARDIOVASCULAR SYSTEMS | SEGMENT | SCN5A MUTATIONS | arrhythmias, cardiac | TRAFFICKING | ion channels | NA(V)1.5 | electrophysiology | GENE | GENETICS & HEREDITY | SUDDEN CARDIAC DEATH | SCN5A protein, human | ASSOCIATION | Brugada Syndrome - genetics | Brugada Syndrome - physiopathology | Humans | Cells, Cultured | Rats | Genotype | NAV1.5 Voltage-Gated Sodium Channel - metabolism | Mutation, Missense | Sodium - metabolism | Rats, Sprague-Dawley | Phenotype | Animals | Brugada Syndrome - metabolism | Electrocardiography | Myocytes, Cardiac - metabolism | NAV1.5 Voltage-Gated Sodium Channel - genetics | Index Medicus | arrhythmia (mechanisms) | SCN5A | ion channel
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7. Full Text Dominant-negative effect of SCN5A N-terminal mutations through the interaction of Nav1.5 α-subunits
by Clatot, Jérôme and Ziyadeh-Isleem, Azza and Maugenre, Svetlana and Denjoy, Isabelle and Liu, Haiyan and Dilanian, Gilles and Hatem, Stéphane N and Deschênes, Isabelle and Coulombe, Alain and Guicheney, Pascale and Neyroud, Nathalie
Cardiovascular Research, ISSN 0008-6363, 10/2012, Volume 96, Issue 1, pp. 53 - 63
1.5 | SCN5A | Arrhythmia | Brugada syndrome | Sodium | Nav1.5 | Original
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8. Full Text A common co-morbiditymodulates disease expression and treatment efficacy in inherited cardiac sodiumchannelopathy
by Rivaud, Mathilde R and Jansen, John A and Postema, Pieter G and Nannenberg, Eline A and Mizusawa, Yuka and Van Der Nagel, Roel and Wolswinkel, Rianne and Van Der Made, Ingeborg and Marchal, Gerard A and Rajamani, Sridharan and Belardinelli, Luiz and Van Tintelen, J. Peter and Tanck, Michael W.T and Van DerWal, Allard C and De Bakker, Jacques M.T and Van Rijen, Harold V and Creemers, Esther E and Wilde, Arthur A.M and Van Den Berg, Maarten P and Van Veen, Toon A.B and Bezzina, Connie R and Remme, Carol Ann
European Heart Journal, ISSN 0195-668X, 08/2018, Volume 39, Issue 31, pp. 2898 - 2907
Hypertension | Ventricular arrhythmias | Conduction delay | Sudden death | Cardiac hypertrophy | SCN5A
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9. Full Text Lack of influence of sex hormones on Brugada syndrome: The role of S-nitrosylation of SCN5A
by Patanè, Salvatore
Journal of electrocardiology, ISSN 0022-0736, 12/2018
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10. Full Text UBC9 regulates cardiac sodium channel Nav1.5 ubiquitination, degradation and sodium current density
by Tang, Bo and Hu, Yushuang and Wang, Pengyun and Wang, Qing Kenneth and Wang, Zhijie and Cheng, Chen and Liang, Lina and Xiong, Hongbo and Luo, Chunyan and Xu, Chengqi and Chen, Qiuyun
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 04/2019, Volume 129, pp. 79 - 91
Voltage-gated sodium channel Na 1.5 is critical for generation and conduction of cardiac action potentials. Mutations and expression level changes of Na 1.5... 
Ubiquitination | SCN5A | UBC9 | Arrhythmia | Nedd4–2 | Nav1.5 sodium channel
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11. Full Text Ethnic Differences in Patients with Brugada Syndrome and Arrhythmic Events: New Insights from SABRUS
by Milman, Anat and Andorin, Antoine and Postema, Pieter G and Gourraud, Jean-Baptiste and Sacher, Frederic and Mabo, Philippe and Kim, Sung-Hwan and Maeda, Shingo and Takahashi, Yoshihide and Kamakura, Tsukasa and Aiba, Takeshi and Conte, Giulio and Juang, Jimmy JM and Leshem, Eran and Michowitz, Yoav and Fogelman, Rami and Hochstadt, Aviram and Mizusawa, Yuka and Giustetto, Carla and Arbelo, Elena and Huang, Zhengrong and Corrado, Domenico and Delise, Pietro and Allocca, Giuseppe and Takagi, Masahiko and Wijeyeratne, Yanushi D and Mazzanti, Andrea and Brugada, Ramon and Casado-Arroyo, Ruben and Champagne, Jean and Calo, Leonardo and Sarquella-Brugada, Georgia and Jespersen, Camilla H and Tfelt-Hansen, Jacob and Veltmann, Christian and Priori, Silvia G and Behr, Elijah R and Yan, Gan-Xin and Brugada, Josep and Gaita, Fiorenzo and Wilde, Arthur A.M and Brugada, Pedro and Kusano, Kengo F and Hirao, Kenzo and Nam, Gi-Byoung and Probst, Vincent and Belhassen, Bernard
Heart Rhythm, ISSN 1547-5271, 07/2019
BACKGROUNDThere is limited information on ethnic differences between patients with Brugada syndrome (BrS) and arrhythmic events (AEs). OBJECTIVEThe purpose of... 
Index Medicus
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12. Full Text SCN5A Variant R222Q generated abnormal changes in cardiac sodium current and action potentials in murine myocytes and Purkinje cells
by Daniel, Laura L and Yang, Tao and Kroncke, Brett and Hall, Lynn and Stroud, Dina and Roden, Dan M
Heart rhythm, ISSN 1547-5271, 05/2019
The cardiac sodium channel (SCN5A) mutation, R222Q, neutralizes a positive charge in the domain I voltage sensor. Mutation carriers display very frequent... 
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13. Full Text Multifocal atrial and ventricular premature contractions with an increased risk of dilated cardiomyopathy caused by a Na(v)1.5 gain-of-function mutation (G213D)
by Calloe, K and Broendberg, AK and Christensen, AH and Pedersen, LN and Olesen, MS and Tejada, MD and Friis, S and Thomsen, MB and Bundgaard, H and Jensen, HK
INTERNATIONAL JOURNAL OF CARDIOLOGY, ISSN 0167-5273, 04/2018, Volume 257, pp. 160 - 167
Background: SCN5A mutations can lead to different cardiac diseases. Recently, SCN5A mutations have been linked to the clinical entity multifocal ectopic... 
FIBRILLATION | CARDIAC & CARDIOVASCULAR SYSTEMS | Arrhythmia | MECHANISM | VARIANTS | SCN5A MUTATIONS | COMPLEXES | CARDIAC SODIUM-CHANNEL | Dilated cardiomyopathy | ECTOPY | LONG QT SYNDROME | SCN5A | Flecainide | Na(v)1.5
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14. Full Text A Novel SCN5A Variant Associated with Abnormal Repolarization, Atrial Fibrillation, and Reversible Cardiomyopathy
by Boddum, Kim and Saljic, Arnela and Jespersen, Thomas and Christensen, Alex Hørby
Cardiology, ISSN 0008-6312, 06/2018, Volume 140, Issue 1, pp. 8 - 13
A variety of life-threating arrhythmias are caused by mutations in the cardiac voltage-gated sodium channel encoded by the SCN5A gene. In this study, we report... 
Short Communication | Cardiomyopathy | Atrial fibrillation | SCN5A | SCN5A MUTATION | BRUGADA-SYNDROME | CARDIAC & CARDIOVASCULAR SYSTEMS | DILATED CARDIOMYOPATHY
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15. Full Text Gene-Specific Therapy With Mexiletine Reduces Arrhythmic Events in Patients With Long QT Syndrome Type 3
by Mazzanti, Andrea, MD and Maragna, Riccardo, BS and Faragli, Alessandro, MD and Monteforte, Nicola, MD and Bloise, Raffaella, MD and Memmi, Mirella, PhD and Novelli, Valeria, PhD and Baiardi, Paola, PhD and Bagnardi, Vincenzo, PhD and Etheridge, Susan P., MD and Napolitano, Carlo, MD, PhD and Priori, Silvia G., MD, PhD
JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2016, Volume 67, Issue 9, pp. 1053 - 1058
Abstract Background Long QT syndrome type 3 (LQT3) is a lethal disease caused by gain-of-function mutations in the SCN5A  gene, coding for the alpha-subunit of... 
Cardiovascular | Internal Medicine | mutation | beta-blocker | SCN5A | sudden cardiac death | sodium channel | CARDIAC & CARDIOVASCULAR SYSTEMS | GENOTYPE | SCN5A MUTATIONS | LQT3 | LINK | NA+ CHANNEL BLOCKADE | ASSOCIATION | Follow-Up Studies | Mexiletine - administration & dosage | Administration, Oral | Humans | Male | Treatment Outcome | Voltage-Gated Sodium Channel Blockers - administration & dosage | Long QT Syndrome - therapy | Long QT Syndrome - physiopathology | Young Adult | Heart Rate - drug effects | Adolescent | Electrocardiography | Long QT Syndrome - genetics | Adult | Female | Retrospective Studies | Child | Genetic Therapy - methods | Long QT syndrome | Care and treatment | Cardiology | Mexiletine | Genes | Confidence intervals | Heart rate | Cardiac arrhythmia | Hypotheses | Statistical analysis | Medical prognosis | Mutation | Drug dosages | Index Medicus | Abridged Index Medicus | CI, confidence interval | LQT3, long QT syndrome type 3 | ECG, electrocardiogram | Original Investigation | LQTS, long QT syndrome
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16. Full Text Multiple mechanisms underlie increased cardiac late sodium current
by Kroncke, Brett M and Yang, Tao and Roden, Dan M
Heart Rhythm, ISSN 1547-5271, 07/2019, Volume 16, Issue 7, pp. 1091 - 1097
We recently reported a quantitative relationship between the degree of functional perturbation reported in the literature for 356 variants in the cardiac... 
Genetics | hiPSC-CMs | SCN5A/NaV1.5 | Late/persistent current | Human-induced pluripotent stem cell cardiomyocytes | LQT3 | INACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | VARIANTS | LONG QT SYNDROME | CHANNEL MUTATIONS | SCN5A/Na(V)1.5 | ANEMONIA-SULCATA | Medicine, Experimental | Medical research | Analysis | Stem cells
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17. Full Text Modeling type 3 long QT syndrome with cardiomyocytes derived from patient-specific induced pluripotent stem cells
by Ma, Dongrui and Wei, Heming and Zhao, Yongxing and Lu, Jun and Li, Guang and Sahib, Norliza Binte Esmail and Tan, Teng Hong and Wong, Keng Yean and Shim, Winston and Wong, Philip and Cook, Stuart A and Liew, Reginald
International Journal of Cardiology, ISSN 0167-5273, 2013, Volume 168, Issue 6, pp. 5277 - 5286
Abstract Background Type 3 long QT syndrome (LQT3) is the third most common form of LQT syndrome and is characterized by QT-interval prolongation resulting... 
Cardiovascular | Long QT syndrome | Cardiomyocytes | Sodium channel | SCN5A | Induced pluripotent stem cells | CARDIAC & CARDIOVASCULAR SYSTEMS | CARDIAC-ARRHYTHMIAS | DISPERSION | SCN5A MUTATIONS | MECHANISMS | CELLULAR-MODEL | REPOLARIZATION | MEXILETINE | DISEASE | CHANNEL MUTATIONS | GENERATION | Pluripotent Stem Cells - cytology | Mexiletine - pharmacology | Myocytes, Cardiac - cytology | Fibroblasts - physiology | Humans | Heart Arrest - genetics | Child, Preschool | Genotype | Heart Arrest - physiopathology | Membrane Potentials - physiology | Long QT Syndrome - physiopathology | Action Potentials - physiology | Chromosomes, Human, Pair 3 | Patch-Clamp Techniques | Myocytes, Cardiac - drug effects | Myocytes, Cardiac - physiology | Electrocardiography | Long QT Syndrome - genetics | Voltage-Gated Sodium Channel Blockers - pharmacology | Female | Fibroblasts - cytology | NAV1.5 Voltage-Gated Sodium Channel - genetics | Dermis - cytology | Child | Models | Analysis | Stem cells | Index Medicus
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18. Full Text Proposed diagnostic criteria for the Brugada syndrome
by Wilde, Arthur A. M and Antzelevitch, C and Borggrefe, M and Brugada, J and Brugada, R and Brugada, P and Corrado, D and Hauer, R.N.W and Kass, R.S and Nademanee, K and Priori, S.G and Towbin, J.A
European Heart Journal, ISSN 0195-668X, 11/2002, Volume 23, Issue 21, pp. 1648 - 1654
ST segment elevation | Cardiac arrhythmias | Genetics | SCN5A | Sudden death
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19. Full Text Multifocal atrial and ventricular premature contractions with an increased risk of dilated cardiomyopathy caused by a Nav1.5 gain-of-function mutation (G213D)
by Calloe, Kirstine and Broendberg, Anders K and Christensen, Alex H and Pedersen, Lisbeth N and Olesen, Morten S and de los Angeles Tejada, Maria and Friis, Soren and Thomsen, Morten B and Bundgaard, Henning and Jensen, Henrik K
International Journal of Cardiology, ISSN 0167-5273, 04/2018, Volume 257, pp. 160 - 167
Background: SCN5A mutations can lead to different cardiac diseases. Recently, SCN5A mutations have been linked to the clinical entity multifocal ectopic... 
Nav1.5 | SCN5A | Arrhythmia | Dilated cardiomyopathy | Flecainide | Index Medicus
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