1.
Mikami A, Imoto K, Tanabe T, Niidome T, Mori Y, Takeshima H, Narumiya S, Numa S.
Primary structure and functional expression of the cardiac dihydropyridine-sensitive calcium
channel. Nature Jul 20 1989;340:230-233.
2.
Yang J, Ellinor PT, Sather WA, Zhang JF, Tsien RW. Molecular determinants of Ca2+
selectivity and ion permeation in L-type Ca2+ channels. Nature Nov 11 1993;366:158-161.
3.
Heinemann SH, Terlau H, Stühmer W, Imoto K, Numa S. Calcium channel characteristics
conferred on the sodium channel by single mutations. Nature Apr 2 1992;356:441-443.
4.
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
Dec 2010;7:1872-1882.
5.
Ye D, Tester DJ, Zhou W, Papagiannis J, Ackerman MJ. A pore-localizing CACNA1CE1115K missense mutation, identified in a patient with idiopathic QT prolongation,
bradycardia, and autism spectrum disorder, converts the L-type calcium channel into a hybrid
nonselective monovalent cation channel. Heart rhythm Feb 2019;16:270-278.
6.
Yamamoto Y, Makiyama T, Harita T, et al. Allele-specific ablation rescues
electrophysiological abnormalities in a human iPS cell model of long-QT syndrome with a
CALM2 mutation. Human molecular genetics May 1 2017;26:1670-1677.
7.
Yoshinaga D, Baba S, Makiyama T, et al. Phenotype-Based High-Throughput Classification
of Long QT Syndrome Subtypes Using Human Induced Pluripotent Stem Cells. Stem Cell
Reports Aug 13 2019;13:394-404.
8.
Horvath B, Banyasz T, Jian Z, Hegyi B, Kistamas K, Nanasi PP, Izu LT, Chen-Izu Y.
Dynamics of the late Na(+) current during cardiac action potential and its contribution to
afterdepolarizations. J Mol Cell Cardiol Nov 2013;64:59-68.
9.
Himeno Y, Asakura K, Cha CY, Memida H, Powell T, Amano A, Noma A. A human
ventricular myocyte model with a refined representation of excitation-contraction coupling.
Biophys J Jul 21 2015;109:415-427.
10.
Schwartz PJ, Priori SG, Locati EH, Napolitano C, Cantù F, Towbin JA, Keating MT,
Hammoude H, Brown AM, Chen LS, Colatsky TJ. Long QT syndrome patients with
mutations of the SCN5A and HERG genes have differential responses to Na+ channel
blockade and to increases in heart rate. Implications for gene-specific therapy. Circulation
Dec 15 1995;92:3381-3386.
11.
Shimizu W, Antzelevitch C. Cellular basis for the ECG features of the LQT1 form of the
long-QT syndrome: effects of beta-adrenergic agonists and antagonists and sodium channel
blockers on transmural dispersion of repolarization and torsade de pointes. Circulation Nov
24 1998;98:2314-2322.
12.
Bos JM, Crotti L, Rohatgi RK, Castelletti S, Dagradi F, Schwartz PJ, Ackerman MJ.
Mexiletine Shortens the QT Interval in Patients With Potassium Channel-Mediated Type 2
Long QT Syndrome. Circ Arrhythm Electrophysiol May 2019;12:e007280.
13.
Gao Y, Xue X, Hu D, Liu W, Yuan Y, Sun H, Li L, Timothy KW, Zhang L, Li C, Yan GX.
Inhibition of late sodium current by mexiletine: a novel pharmotherapeutical approach in
timothy syndrome. Circ Arrhythm Electrophysiol Jun 2013;6:614-622.
14.
Badri M, Patel A, Patel C, Liu G, Goldstein M, Robinson VM, Xue X, Yang L, Kowey PR,
Yan GX. Mexiletine Prevents Recurrent Torsades de Pointes in Acquired
Long QT Syndrome Refractory to Conventional Measures. JACC Clin Electrophysiol Aug
2015;1:315-322.
15.
Makita N, Behr E, Shimizu W, et al. The E1784K mutation in SCN5A is associated with
mixed clinical phenotype of type 3 long QT syndrome. J Clin Invest Jun 2008;118:22192229.
16.
Bezzina C, Veldkamp MW, van Den Berg MP, Postma AV, Rook MB, Viersma JW, van
Langen IM, Tan-Sindhunata G, Bink-Boelkens MT, van Der Hout AH, Mannens MM, Wilde
AA. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. Circ
Res Dec 3-17 1999;85:1206-1213.
17.
Shryock JC, Song Y, Rajamani S, Antzelevitch C, Belardinelli L. The arrhythmogenic
consequences of increasing late INa in the cardiomyocyte. Cardiovasc Res Sep 1
2013;99:600-611.
18.
Wu L, Ma J, Li H, Wang C, Grandi E, Zhang P, Luo A, Bers DM, Shryock JC, Belardinelli
L. Late sodium current contributes to the reverse rate-dependent effect of IKr inhibition on
ventricular repolarization. Circulation Apr 26 2011;123:1713-1720.
19.
Guo D, Lian J, Liu T, Cox R, Margulies KB, Kowey PR, Yan GX. Contribution of late
sodium current (I(Na-L)) to rate adaptation of ventricular repolarization and reverse usedependence of QT-prolonging agents. Heart rhythm May 2011;8:762-769.
20.
Maltsev VA, Undrovinas AI. A multi-modal composition of the late Na+ current in human
ventricular cardiomyocytes. Cardiovasc Res Jan 2006;69:116-127.
21.
Viatchenko-Karpinski S, Kornyeyev D, El-Bizri N, Budas G, Fan P, Jiang Z, Yang J,
Anderson ME, Shryock JC, Chang CP, Belardinelli L, Yao L. Intracellular Na+ overload
causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.
J Mol Cell Cardiol Nov 2014;76:247-256.
22.
Xi J, Khalil M, Shishechian N, et al. Comparison of contractile behavior of native murine
ventricular tissue and cardiomyocytes derived from embryonic or induced pluripotent stem
cells. Faseb j Aug 2010;24:2739-2751.
23.
Hess P, Lansman JB, Tsien RW. Calcium channel selectivity for divalent and monovalent
cations. Voltage and concentration dependence of single channel current in ventricular heart
cells. The Journal of general physiology Sep 1986;88:293-319.
...