16 Schram G, Pourrier M, Wang Z, et al. Barium block of Kir2 and human cardiac inward rectifier currents: evidence for subunit-heteromeric contribution to native currents. Cardiovasc Res, 2003, 59: 328-338
[2]
17 Preisig-Muller R, Schlichthorl G, Goerge T, et, al. Heteromerization of Kir2.x potassium channels contributes to the phenotype of Andersen’s syndrome. Proc Natl Acad Sci USA, 2002, 99: 7774-7779
[3]
18 Zobel C, Cho H C, Nguyen T T, et al. Molecular dissection of the inward rectifier potassium current (IK1) in rabbit cardiomyocytes: evidence for heteromeric coassembly of Kir2.1 and Kir2.2. J Physiol. 2003, 550: 365-372
[4]
19 Caballero R, Dolz-Gaitón P, Gómez R, et al. Flecainide increases Kir2.1 currents by interacting with cysteine 311, decreasing the polyamine-induced rectification. Proc Natl Acad Sci USA, 2010, 107: 15631-15636
[5]
20 Dart C, Leyland M L. Targeting of an A kinase-anchoring protein, AKAP79, to an inwardly rectifying potassium channel, Kir2.1. J Biol Chem, 2001, 276: 20499-20505
[6]
21 Leonoudakis D, Conti L R, Anderson S, et al. Protein trafficking and anchoring complexes revealed by proteomic analysis of inward rectifier potassium channel (Kir2.x)-associated proteins. J Biol Chem, 2004, 279: 22331-22346
[7]
22 Thomas P, Smart T G. HEK293 cell line: a vehicle for the expression of recombinant proteins. J Pharmacol Toxicol Method, 2005, 51: 187-200
[8]
23 Mazzanti M, Assandri R, Ferroni A, et al. Cytoskeletal control of rectification and expression of four substates in cardiac inward rectifier K channels. FASEB J, 1996, 10: 357-361
[9]
1 Lopatin A N, Nichols C G. Inward rectifiers in the heart: an update on IK1. J Mol Cell Cardiol, 2001, 33: 625-638
[10]
2 Liu Q H, Li X L, Xu Y W, et al. A novel discovery of IK1 channel agonist: zacopride selectively enhances IK1 current and suppresses triggered arrhythmias in the rat. J Cardiovasc Pharmacol, 2012, 59: 37-48
[11]
3 Nagakura Y, Akuzawa S, Miyata K, et al. Pharmacological properties of a novel gastrointestinal prokinetic benzamide selective for human 5-HT4 receptor versus human 5-HT3 receptor. Pharmacol Res, 1999, 39: 375-382
[12]
4 Yusuf S, Al-Saady N, Camm A J. 5-hydroxytryptamine and atrial fibrillation: how significant is this piece in the puzzle? J Cardiovasc Electrophysiol, 2003, 14: 209-214
[13]
5 Berlin J R, Cannell M B, Lederer W J. Cellular origins of the transient inward current in cardiac myocytes. Role of fluctuations and waves of elevated intracellular calcium. Circ Res, 1989, 65: 115-126
[14]
6 Pino R, Cerbai E, Calamai G, et al. Effect of 5-HT4 receptor stimulation on the pacemaker current If in human isolated atrial myocytes. Cardiovasc Res, 1998, 40: 516-522
[15]
7 Sridhar A, Nishijima Y, Terentyev D, et al. Chronic heart failure and the substrate for atrial fibrillation. Cardiovasc Res, 2009, 84: 227-236
[16]
8 Gaborit N, Steenman M, Lamirault G, et al. Human atrial ion channel and transporter subunit gene-expression remodeling associated with valvular heart disease and atrial fibrillation. Circulation, 2005, 112: 471-481
[17]
9 Li J D, McLerie M, Lopatin A N. Transgenic upregulation of IK1 in the mouse heart leads to multiple abnormalities of cardiac excitability. Am J Physiol Heart C, 2004, 287: H2790-H2802
[18]
10 Anumonwo J M, Lopatin A N. Cardiac strong inward rectifier potassium channels. J Mol Cell Cardio, 2009, 48: 45-54
[19]
11 Hibino H, Inanobe A, Furutain K, et al. Inwardly rectifying potassium channels: their structure, function, and physiological roles. Physiol Rev, 2010, 90: 291-366
[20]
12 Karschin A. G protein regulation of inwardly rectifying K+ channels. News Physiol Sci, 1999, 14: 215-220
[21]
13 Mubagwa K, Stengl M, Flameng W. Extracellular divalent cations block a cation non-selective conductance unrelated to calcium channels in cardiac cells. J Physiol, 1997, 502: 235-247
[22]
14 Wittenberg B A, Robinson T F. Oxygen requirements, morphology, cell coat and membrane permeability of calcium-tolerant myocytes from hearts of adult rats. Cell Tissue Res, 1981, 216: 231-251
[23]
15 Wischmeyer E, Karschin A. Receptor stimulation causes slow inhibition of IRK1 inwardly rectifying K+ channels by direct protein kinase A-mediated Phosphorylation. Proc Natl Acad Sci USA, 1996, 93: 5819-5823