Molecular basis of the delayed rectifier current I(ks)in heart.

Détails

ID Serval
serval:BIB_82B2C64C8F07
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Molecular basis of the delayed rectifier current I(ks)in heart.
Périodique
Journal of Molecular and Cellular Cardiology
Auteur(s)
Kurokawa J., Abriel H., Kass R.S.
ISSN
0022-2828
Statut éditorial
Publié
Date de publication
2001
Peer-reviewed
Oui
Volume
33
Numéro
5
Pages
873-882
Langue
anglais
Notes
Journal Article Review --- Old month value: May
Résumé
J. Kurokawa, H. Abriel and R. S. Kass. Molecular Basis of the Delayed Rectifier Current I(Ks)in Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 873-882. Electrical activity underlies the control of the frequency, strength, and duration of contraction of the heart. During the cardiac cycle, a regular rhythmic pattern must be established in time-dependent changes in ionic conductances in order to ensure events that underlie normal cardiac function. This pattern must be tightly regulated by sympathetic nervous activity to ensure a physiologically relevant relationship between diastolic filling and ejection times with variable heart rate. The duration of the ventricular action potential is controlled in part by a slowly activated potassium channel current, I(Ks). The molecular identity of the subunits that comprise the channels conducting this current is important, not only for understanding the fundamental mechanisms that control electrical activity in healthy individuals, but also for understanding the molecular basis of at least one inherited human disease, LQTS-1. This brief review summarizes key points of information regarding the molecular determinants of the activity of these channels, their relationship to human disease, and what is known, and yet to be discovered, about the molecular determinants of the regulation of this channel by sympathetic nervous activity.
Mots-clé
Animals, Arrhythmias, Cardiac, Cadmium, Cell Membrane, Guinea Pigs, Humans, KCNQ Potassium Channels, KCNQ1 Potassium Channel, Kinetics, Long QT Syndrome, Potassium Channels, Potassium Channels, Voltage-Gated, Protein Kinases, Protein Structure, Tertiary, Time Factors
Pubmed
Web of science
Création de la notice
24/01/2008 10:56
Dernière modification de la notice
20/08/2019 14:42
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