Regulation of the voltage-gated cardiac sodium channel Nav1.5 by interacting proteins.

Détails

ID Serval
serval:BIB_ED033A4BCEBA
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
Regulation of the voltage-gated cardiac sodium channel Nav1.5 by interacting proteins.
Périodique
Trends in Cardiovascular Medicine
Auteur⸱e⸱s
Abriel H., Kass R.S.
ISSN
1050-1738
Statut éditorial
Publié
Date de publication
2005
Peer-reviewed
Oui
Volume
15
Numéro
1
Pages
35-40
Langue
anglais
Résumé
Na(v)1.5, the major cardiac voltage-gated Na(+) channel, plays a central role in the generation of the cardiac action potential and in the propagation of electrical impulses in the heart. Its importance for normal heart function has been recently exemplified by reports of numerous mutations found in the gene SCN5A--which encodes Na(v)1.5--in patients with various pathologic cardiac phenotypes, indicating that even subtle alterations of Na(v)1.5 cell biology and function may underlie human diseases. Similar to other ion channels, Na(v)1.5 is most likely part of dynamic multiprotein complexes located in the different cellular compartments. This review focuses on five intracellular proteins that have been recently reported to directly bind to and contribute to the regulation of Na(v)1.5: ankyrin proteins, fibroblast growth factor homologous factor 1B, calmodulin, Nedd4-like ubiquitin-protein ligases, and syntrophin proteins.
Mots-clé
Cell Line, Gene Expression Regulation, Humans, Ion Channel Gating, Ion Transport, Muscle Proteins, Myocardium, Myocytes, Cardiac, Protein Processing, Post-Translational, Sodium Channels, Ubiquitin, Ubiquitin-Protein Ligases
Pubmed
Web of science
Création de la notice
24/01/2008 11:56
Dernière modification de la notice
20/08/2019 17:14
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