Sodium channel protein type 5 subunit alpha

[1]. Sandra B Gabelli, et al. Regulation of the NaV1.5 cytoplasmic domain by calmodulin. Nat Commun. 2014 Nov 5;5:5126. [Content Brief]

[2]. Darouna Kattygnarath, et al. MOG1: a new susceptibility gene for Brugada syndrome. Circ Cardiovasc Genet. 2011 Jun;4(3):261-8. [Content Brief]

[3]. Lumin Wang, et al. De Novo Mutation in the SCN5A Gene Associated with Brugada Syndrome. Cell Physiol Biochem. 2015;36(6):2250-62. [Content Brief]

[4]. Benjamin Chagot, et al. Solution NMR structure of the C-terminal EF-hand domain of human cardiac sodium channel NaV1.5. J Biol Chem. 2009 Mar 6;284(10):6436-45. [Content Brief]

[5]. Lucía Núñez, et al. p.D1690N Nav1.5 rescues p.G1748D mutation gating defects in a compound heterozygous Brugada syndrome patient. Heart Rhythm. 2013 Feb;10(2):264-72. [Content Brief]

[6]. Zhipeng Zeng, et al. Electrophysiological characteristics of a SCN5A voltage sensors mutation R1629Q associated with Brugada syndrome. PLoS One. 2013 Oct 22;8(10):e78382. [Content Brief]

[7]. Koshi Kinoshita, et al. SCN5A(K817E), a novel Brugada syndrome-associated mutation that alters the activation gating of NaV1.5 channel. Heart Rhythm. 2016 May;13(5):1113-1120. [Content Brief]

[8]. Hassan Musa, et al. SCN5A variant that blocks fibroblast growth factor homologous factor regulation causes human arrhythmia. Proc Natl Acad Sci U S A. 2015 Oct 6;112(40):12528-33. [Content Brief]

[9]. Susmita Chakrabarti, et al. MOG1 rescues defective trafficking of Na(v)1.5 mutations in Brugada syndrome and sick sinus syndrome. Circ Arrhythm Electrophysiol. 2013 Apr;6(2):392-401. [Content Brief]

[10]. M E Gellens, et al. Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel. Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):554-8. [Content Brief]