Sodium Current and Potassium Transient Outward Current Genes in Brugada Syndrome: Screening and Bioinformatics

Canadian Journal of Cardiology

Volumn 28, Issue 2, 2012, Pages 196-200

  Holst, Anders G ^a,b   Saber, Siamak ^c   Houshmand, Massoud ^d   Zaklyazminskaya, Elena V ^e   Wang, Yinman ^a,b   Jensen, Henrik Kjærulf ^f   Refsgaard, Lena ^a,b   Haunsø, Stig ^a,b,g   Svendsen, Jesper Hastrup ^a,b,g   Olesen, Morten S ^a,b   Tfelt Hansen, Jacob ^a,b  

^a DANISH NATIONAL RESEARCH FOUNDATION   (Denmark)

^b UNIVERSITY OF COPENHAGEN   (Denmark)

^c Special Medical Centre   (Iran)

^d NATIONAL INSTITUTE OF GENETIC ENGINEERING AND BIOTECHNOLOGY   (Iran)

^e PETROVSKY NATIONAL RESEARCH CENTER OF SURGERY   (Russian Federation)

^f AARHUS UNIVERSITY HOSPITAL   (Denmark)

^g UNIVERSITY OF COPENHAGEN   (Denmark)

Author keywords

[No Author keywords available]

Indexed keywords

CAV3 PROTEIN; MOG1 PROTEIN; POTASSIUM; POTASSIUM CHANNEL; POTASSIUM CHANNEL KCND3; SODIUM; SODIUM CHANNEL; SODIUM CHANNEL SCN1B; SODIUM CHANNEL SCN4B; UNCLASSIFIED DRUG;

ADULT; ALLELE; ARTICLE; BIOINFORMATICS; BRUGADA SYNDROME; CLINICAL ARTICLE; CONTROLLED STUDY; EXOME; EXON; FEMALE; GENE SEQUENCE; GENETIC ASSOCIATION; GENETIC SCREENING; GENETIC VARIABILITY; HUMAN; MALE; NONSENSE MUTATION; POTASSIUM CURRENT; SINGLE NUCLEOTIDE POLYMORPHISM; SODIUM CURRENT;

ADULT; BRUGADA SYNDROME; COMPUTATIONAL BIOLOGY; FEMALE; GENETIC TESTING; HUMANS; MALE; MIDDLE AGED; POTASSIUM; SODIUM; SODIUM CHANNELS;

EID: 84862776540     PISSN: 0828282X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.cjca.2011.11.011     Document Type: Article

References (21)

1. Antzelevitch C., Brugada P., Borggrefe M., et al. Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation 2005, 111:659-670.
2. Probst V., Veltmann C., Eckardt L., et al. Long-term prognosis of patients diagnosed with Brugada syndrome: results from the FINGER Brugada syndrome registry. Circulation 2010, 121:635-643.
3. Brugada J., Brugada R., Antzelevitch C., Towbin J., Nademanee K., Brugada P. Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3. Circulation 2002, 105:73-78.
4. Sarkozy A., Boussy T., Kourgiannides G., et al. Long-term follow-up of primary prophylactic implantable cardioverter-defibrillator therapy in Brugada syndrome. Eur Heart J 2007, 28:334-344.
5. Brugada P., Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 1992, 20:1391-1396.
6. Hu D., Barajas-Martinez H., Burashnikov E., et al. A mutation in the {beta}3 subunit of the cardiac sodium channel associated with Brugada ECG phenotype. Circ Cardiovasc Genet 2009, 2:270-278.
7. Antzelevitch C. Genetic basis of Brugada syndrome. Heart Rhythm 2007, 4:756-757.
8. Burashnikov E., Pfeiffer R., Barajas-Martinez H., et al. Mutations in the cardiac L-type calcium channel associated with inherited J wave syndromes and sudden cardiac death. Heart Rhythm 2010, 12:1872-1882.
9. Giudicessi J.R., Ye D., Tester D.J., et al. Transient outward current (Ito) gain-of-function mutations in the KCND3-encoded Kv4.3 potassium channel and Brugada syndrome. Heart Rhythm 2011, 8:1024-1032.
10. Watanabe H., Koopmann T.T., Le Scouarnec S., et al. Sodium channel beta1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans. J Clin Invest 2008, 118:2260-2268.
11. London B., Michalec M., Mehdi H., et al. Mutation in glycerol-3-phosphate dehydrogenase 1-like gene (GPD1-L) decreases cardiac Na+ current and causes inherited arrhythmias. Circulation 2007, 116:2260-2268.
12. Kattygnarath D., Maugenre S., Neyroud N., et al. MOG1: a new susceptibility gene for Brugada syndrome. Circ Cardiovasc Genet 2011, 4:261-268.
13. Deschênes I., Tomaselli G.F. Modulation of Kv4.3 current by accessory subunits. FEBS Letters 2002, 528:183-188.
14. Deschênes I., Armoundas A.A., Jones S.P., Tomaselli G.F. Post-transcriptional gene silencing of KChIP2 and Nav[beta]1 in neonatal rat cardiac myocytes reveals a functional association between Na and Ito currents. J Mol Cell Cardiol 2008, 45:336-346.
15. Vatta M., Ackerman M.J., Ye B., et al. Mutant caveolin-3 induces persistent late sodium current and is associated with long-QT syndrome. Circulation 2006, 114:2104-2112.
16. Cronk L.B., Ye B., Kaku T., et al. Novel mechanism for sudden infant death syndrome: persistent late sodium current secondary to mutations in caveolin-3. Heart Rhythm 2007, 4:161-166.
17. Delpon E., Cordeiro J.M., Nunez L., et al. Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome. Circ Arrhythmia Electrophysiol 2008, 1:209-218.
18. Exome Sequencing Project National Heart, Lung, and Blood Institute, Accessed November 22, 2011. http://evs.gs.washington.edu/EVS/.
19. Koopmann T.T., Beekman L., Alders M., et al. Exclusion of multiple candidate genes and large genomic rearrangements in SCN5A in a Dutch Brugada syndrome cohort. Heart Rhythm 2007, 4:752-755.
20. Antzelevitch C., Pollevick G.D., Cordeiro J.M., et al. Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death. Circulation 2007, 115:442-449.
21. Olesen M.S., Jensen N.F., Holst A.G., et al. A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias. Can J Cardiol 2011, 27:523.e17-523.e23.