Similar articles for PMID: 11804990

Year	Number of Results
1995	1
1996	1
1998	4
1999	3
2000	5
2001	8
2002	9
2003	11
2004	6
2005	5
2006	9
2007	10
2008	7
2009	6
2010	8
2011	8
2012	9
2013	4
2014	3
2015	5
2016	3
2017	2
2018	3
2019	3
2020	1
2021	2
2022	1
2024	0

1

Clinical, genetic, and biophysical characterization of SCN5A mutations associated with atrioventricular conduction block.

Wang DW, Viswanathan PC, Balser JR, George AL Jr, Benson DW. Wang DW, et al. Circulation. 2002 Jan 22;105(3):341-6. doi: 10.1161/hc0302.102592. Circulation. 2002. PMID: 11804990

2

A heterozygous deletion mutation in the cardiac sodium channel gene SCN5A with loss- and gain-of-function characteristics manifests as isolated conduction disease, without signs of Brugada or long QT syndrome.

Zumhagen S, Veldkamp MW, Stallmeyer B, Baartscheer A, Eckardt L, Paul M, Remme CA, Bhuiyan ZA, Bezzina CR, Schulze-Bahr E. Zumhagen S, et al. PLoS One. 2013 Jun 28;8(6):e67963. doi: 10.1371/journal.pone.0067963. Print 2013. PLoS One. 2013. PMID: 23840796 Free PMC article.

3

Novel SCN5A mutation leading either to isolated cardiac conduction defect or Brugada syndrome in a large French family.

Kyndt F, Probst V, Potet F, Demolombe S, Chevallier JC, Baro I, Moisan JP, Boisseau P, Schott JJ, Escande D, Le Marec H. Kyndt F, et al. Circulation. 2001 Dec 18;104(25):3081-6. doi: 10.1161/hc5001.100834. Circulation. 2001. PMID: 11748104

4

Homozygous SCN5A mutation in long-QT syndrome with functional two-to-one atrioventricular block.

Lupoglazoff JM, Cheav T, Baroudi G, Berthet M, Denjoy I, Cauchemez B, Extramiana F, Chahine M, Guicheney P. Lupoglazoff JM, et al. Circ Res. 2001 Jul 20;89(2):E16-21. doi: 10.1161/hh1401.095087. Circ Res. 2001. PMID: 11463728

5

Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel.

Wei J, Wang DW, Alings M, Fish F, Wathen M, Roden DM, George AL Jr. Wei J, et al. Circulation. 1999 Jun 22;99(24):3165-71. doi: 10.1161/01.cir.99.24.3165. Circulation. 1999. PMID: 10377081

6

A sodium channel pore mutation causing Brugada syndrome.

Pfahnl AE, Viswanathan PC, Weiss R, Shang LL, Sanyal S, Shusterman V, Kornblit C, London B, Dudley SC Jr. Pfahnl AE, et al. Heart Rhythm. 2007 Jan;4(1):46-53. doi: 10.1016/j.hrthm.2006.09.031. Epub 2006 Sep 28. Heart Rhythm. 2007. PMID: 17198989 Free PMC article.

7

A homozygous SCN5A mutation in a severe, recessive type of cardiac conduction disease.

Neu A, Eiselt M, Paul M, Sauter K, Stallmeyer B, Isbrandt D, Schulze-Bahr E. Neu A, et al. Hum Mutat. 2010 Aug;31(8):E1609-21. doi: 10.1002/humu.21302. Hum Mutat. 2010. PMID: 20564468

8

Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome.

Rook MB, Bezzina Alshinawi C, Groenewegen WA, van Gelder IC, van Ginneken AC, Jongsma HJ, Mannens MM, Wilde AA. Rook MB, et al. Cardiovasc Res. 1999 Dec;44(3):507-17. doi: 10.1016/s0008-6363(99)00350-8. Cardiovasc Res. 1999. PMID: 10690282

9

Novel pore mutation in SCN5A manifests as a spectrum of phenotypes ranging from atrial flutter, conduction disease, and Brugada syndrome to sudden cardiac death.

Rossenbacker T, Carroll SJ, Liu H, Kuipéri C, de Ravel TJ, Devriendt K, Carmeliet P, Kass RS, Heidbüchel H. Rossenbacker T, et al. Heart Rhythm. 2004 Nov;1(5):610-5. doi: 10.1016/j.hrthm.2004.07.001. Heart Rhythm. 2004. PMID: 15851228

10

A novel mutation in SCN5A, delQKP 1507-1509, causing long QT syndrome: role of Q1507 residue in sodium channel inactivation.

Keller DI, Acharfi S, Delacrétaz E, Benammar N, Rotter M, Pfammatter JP, Fressart V, Guicheney P, Chahine M. Keller DI, et al. J Mol Cell Cardiol. 2003 Dec;35(12):1513-21. doi: 10.1016/j.yjmcc.2003.08.007. J Mol Cell Cardiol. 2003. PMID: 14654377

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