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Nav1.5 N-terminal domain binding to α1-syntrophin increases membrane density of human Kir2.1, Kir2.2 and Nav1.5 channels.
Matamoros, Marcos; Pérez-Hernández, Marta; Guerrero-Serna, Guadalupe; Amorós, Irene; Barana, Adriana; Núñez, Mercedes; Ponce-Balbuena, Daniela; Sacristán, Sandra; Gómez, Ricardo; Tamargo, Juan; Caballero, Ricardo; Jalife, José; Delpón, Eva.
Afiliação
  • Matamoros M; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Pérez-Hernández M; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Guerrero-Serna G; Department of Internal Medicine, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109, USA Department of Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109, USA.
  • Amorós I; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Barana A; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Núñez M; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Ponce-Balbuena D; Department of Internal Medicine, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109, USA Department of Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109, USA.
  • Sacristán S; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Gómez R; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Tamargo J; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
  • Caballero R; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain rcaballero@med.ucm.es.
  • Jalife J; Department of Internal Medicine, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109, USA Department of Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109, USA.
  • Delpón E; Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Cardiovasc Res ; 110(2): 279-90, 2016 May 15.
Article em En | MEDLINE | ID: mdl-26786162
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Limite: Animals / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Limite: Animals / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article