Regulation of the cardiac sodium channel Nav1.5 by utrophin in dystrophin-deficient mice

Albesa, Maxime; Ogrodnik, Jakob; Rougier, Jean-Sébastien; Abriel, Hugues (2011). Regulation of the cardiac sodium channel Nav1.5 by utrophin in dystrophin-deficient mice. Cardiovascular research, 89(2), pp. 320-8. Oxford: Oxford University Press 10.1093/cvr/cvq326

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Duchenne muscular dystrophy (DMD) is a severe striated muscle disease due to the absence of dystrophin. Dystrophin deficiency results in dysfunctional sodium channels and conduction abnormalities in hearts of mdx mice. Disease progression in the mdx mouse only modestly reflects that of DMD patients, possibly due to utrophin up-regulation. Here, we investigated mice deficient in both dystrophin and utrophin [double knockout (DKO)] to assess the role of utrophin in the regulation of the cardiac sodium channel (Na(v)1.5) in mdx mice.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DBMR Forschung Mu35 > Forschungsgruppe Ionenkanalkrankheiten
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DBMR Forschung Mu35 > Forschungsgruppe Ionenkanalkrankheiten

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Physiology

UniBE Contributor:

Albesa, Maxime; Ogrodnik, Jakob; Rougier, Jean-Sébastien and Abriel, Hugues

ISSN:

0008-6363

Publisher:

Oxford University Press

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:20

Last Modified:

27 Apr 2018 09:15

Publisher DOI:

10.1093/cvr/cvq326

PubMed ID:

20952415

Web of Science ID:

000286216900011

BORIS DOI:

10.7892/boris.6860

URI:

https://boris.unibe.ch/id/eprint/6860 (FactScience: 211899)

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