A defect in the Kv channel-interacting protein 2 (KChIP2) gene leads to a complete loss of Ito and confers susceptibility to ventricular tachycardia

Cell

Volumn 107, Issue 6, 2001, Pages 801-813

  Kuo, Hai Chien ^a   Cheng, Ching Feng ^a   Clark, Robert B ^b   Lin, Jim J C ^c   Lin, Jenny L C ^c   Hoshijima, Masahiko ^a   Nguye Trân, Vân T B ^a   Gu, Yusu ^a   Ikeda, Yasuhiro ^a   Chu, Po Hsien ^a   Ross Jr , John ^a   Giles, Wayne R ^b   Chien, Kenneth R ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALGARY   (Canada)

^c UNIVERSITY OF IOWA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

KV CHANNEL INTERACTING PROTEIN 2; POTASSIUM CHANNEL; PROTEIN; PROTEIN SUBUNIT; UNCLASSIFIED DRUG;

ACTION POTENTIAL; ANIMAL TISSUE; ARRHYTHMOGENESIS; ARTICLE; CONTROLLED STUDY; GENETIC SUSCEPTIBILITY; HEART FUNCTION; HEART VENTRICLE HYPERTROPHY; HEART VENTRICLE TACHYCARDIA; MOUSE; NONHUMAN; POTASSIUM CURRENT; PRIORITY JOURNAL; PROTEIN EXPRESSION; ST SEGMENT;

ANIMALIA;

EID: 18244408825     PISSN: 00928674     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0092-8674(01)00588-8     Document Type: Article

References (33)

1. Modulation of A-type potassium channels by a family of calcium sensors
2. Basic mechanisms of reentrant arrhythmias
3. The Brugada syndrome: Diagnostic criteria and cellular mechanisms
4. Conserved N-terminal Kv4 domain critical for effects of KChIP2.2 on channel expression and gating
5. Enhanced dispersion of repolarization and refractoriness in transgenic mouse hearts promotes reentrant ventricular tachycardia
6. + channels?
7. Functional knockout of the transient outward current, long-QT syndrome, and cardiac remodeling in mice expressing a dominant-negative Kv4 alpha subunit
8. In vivo cardiac electrophysiology studies in the mouse
9. Electrophysiological abnormalities and arrhythmias in αMHC mutant familial hypertrophic cardiomyopathy mice
10. + currents in isolated human ventricular myocytes from patients with terminal heart failure
11. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation
12. Stress pathways and heart failure
13. Genomic circuits and the integrative biology of cardiac diseases
14. + channel in ventricular muscle. A molecular correlate for the transient outward current
15. Torsades de pointes
16. + current modulates repolarization and excitation-contraction coupling in adult mouse ventricle
17. + channel inactivation, spike broadening, and after-hyperpolarization in Kvbeta1.1-deficient mice with impaired learning
18. Signaling pathways for cardiac hypertrophy and failure
19. Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure
20. Molecular and cellular mechanisms of cardiac arrhythmias
21. Regional differences in current density and rate-dependent properties of the transient outward current in subepicardial and subendocardial myocytes of human left ventricle
22. + channel diversity in the mammalian myocardium
23. A novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages
24. + channels altered by presence of beta-subunit
25. Regulation of KChIP2 potassium channel subunit gene expression underlies the gradient of transient outward current in canine and human ventricle
26. + channel surface expression through effects early in biosynthesis
27. Expression of the Mf1 gene in developing mouse hearts: Implication in the development of human congenital heart defects
28. Electrophysiological remodeling in hypertrophy and heart failure
29. Diminished transient outward currents in rat hypertrophied ventricular myocytes
30. + channel regulatory protein, KChAP
31. + channel subunit in the mouse heart
32. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation
33. Sudden cardiac death