The consequences of disrupting cardiac in wardly rectifying K+ current (IK1) as revealed by the targeted deletion of the murine Kir2.1 and Kir2.2 genes

Journal of Physiology

Volumn 533, Issue 3, 2001, Pages 697-710

  Zaritsky, Joshua J ^a   Redell, John B ^a   Tempel, Bruce L ^b   Schwarz, Thomas L ^a,c  

^a STANFORD UNIVERSITY   (United States)

^b UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

^c BOSTON CHILDREN S HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BARIUM ION; GENE PRODUCT; KIR 2.1 PROTEIN; KIR 2.2 PROTEIN; POTASSIUM ION; UNCLASSIFIED DRUG; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR2.1;

ACTION POTENTIAL; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BIRTH; BRADYCARDIA; CELL MUTANT; CLEFT PALATE; CONTROLLED STUDY; DEATH; ELECTROCARDIOGRAM; EXTRASYSTOLE; GENE DELETION; HEART AUTOMATICITY; HEART MUSCLE CELL; HEART PACING; HEART VENTRICLE WALL; INTRACELLULAR RECORDING; ION CURRENT; MOUSE; MUTATION; NEWBORN; NONHUMAN; PHENOTYPE; POTASSIUM CURRENT; PRIORITY JOURNAL; REENTRY ARRHYTHMIA; SINUS RHYTHM; SLOW INWARD CURRENT; GENE EXPRESSION; GENE TARGETING; GENETIC CODE; HEART RATE; KIR2.1 GENE; KIR2.2 GENE; MUSCLE CELL; REGULATOR GENE; UPREGULATION;

ACTION POTENTIALS; ANIMALS; ANIMALS, NEWBORN; CALCIUM; ELECTRIC CONDUCTIVITY; ELECTROCARDIOGRAPHY; GENE DELETION; HEART VENTRICLES; MICE; MICE, INBRED STRAINS; MICE, KNOCKOUT; MYOCARDIUM; PHENOTYPE; POTASSIUM CHANNELS; POTASSIUM CHANNELS, INWARDLY RECTIFYING; REACTION TIME; REFERENCE VALUES; RNA;

EID: 0035875149     PISSN: 00223751     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1469-7793.2001.t01-1-00697.x     Document Type: Article

References (51)

1. + channels?
2. Functional knockout of the transient outward current, long-QT syndrome, and cardiac remodeling in mice expressing a dominant-negative Kv4 α subunit
3. + channel mRNA in isolated ferret cardiac myocytes
4. + channels and control of ventricular repolarization in the heart
5. Developmental changes in ionic channel activity in the embryonic murine heart
6. Molecular physiology of cardiac potassium channels
7. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats
8. + channel in ventricular muscle. A molecular correlate for the transient outward current
9. + channels in aortic endothelial cells
10. + channels is caused by intracellular spermine
11. + channels
12. + channel proteins via their N-terminal end
13. Comparison of potassium currents in rabbit atrial and ventricular cells
14. Barium-induced automatic activity in isolated ventricular myocytes from guinea-pig hearts
15. Differential distribution of classical inwardly rectifying potassium channel mRNAs in the brain: Comparison of IRK2 with IRK1 and IRK3
16. + currents in fetal, neonatal, and adult rabbit ventricular myocytes
17. + current during the action potential of guinea pig ventricular myocytes
18. Time-dependent outward currents through the inward rectifier potassium channel IRK1. The role of weak blocking molecules
19. + channel in guinea-pig cardiac myocytes
20. Inwardly rectifying potassium channels: Their molecular heterogeneity and function
21. + channel mRNAs are differentially expressed in the adult rat brain
22. +-channel proteins
23. Primary structure and functional expression of a mouse inward rectifier potassium channel
24. Voltage-dependent activation of the inward-rectifier potassium channel in the ventricular cell membrane of guinea-pig heart
25. Long QT and ventricular arrhythmias in transgenic mice expressing the N terminus and first transmembrane segment of a voltage-gated potassium channel
26. The mechanism of inward rectification of potassium channels: "Long-pore plugging" by cytoplasmic polyamines
27. Open-state substructure of inwardly rectifying potassium channels revealed by magnesium block in guinea-pig heart cells
28. + channels in guinea-pig heart cells
29. 2+
30. Inwardly rectifying potassium current in rat fetal and neonatal ventricular cardiomyocytes
31. Molecular cloning and functional expression of a novel brain-specific inward rectifier potassium channel
32. Inhibition of rat ventricular IK1 with antisense oligonucleotides targeted to Kir2.1 mRNA
33. Inward rectification and implications for cardiac excitability
34. Ionic mechanisms controlling the action potential duration and the timing of repolarization
35. Resting K conductances in pacemaker and nonpacemaker heart cells of the rabbit
36. Electrophysiological properties of neonatal mouse cardiac myocytes in primary culture
37. Conductance properties of single inwardly rectifying potassium channels in ventricular cells from guinea-pig heart
38. Depletion of intracellular polyamines relieves inward rectification of potassium channels
39. 2+
40. Molecular cloning and functional expression of cDNA encoding a second class of inward rectifier potassium channels in the mouse brain
41. Regions responsible for the assembly of inwardly rectifying potassium channels
42. + inward rectifier channel associated with motoneurons of cranial nerve nuclei
43. 2+ induced automaticity in guinea pig cardiac myocytes
44. Inward rectification of a potassium channel in cardiac ventricular cells depends on internal magnesium ions
45. The impact of single cell voltage clamp on the understanding of the cardiac ventricular action potential
46. Developmental increases in the inwardly rectifying potassium current of rat ventricular myocytes
47. + channel currents in rat ventricular myocytes
48. Determination of the subunit stoichiometry of an inwardly rectifying potassium channel
49. +-mediated vasodilation