Pannexin-1 Deficient Mice Have an Increased Susceptibility for Atrial Fibrillation and Show a QT-Prolongation Phenotype | Zendy

Stella Petric | Zendy; Sofia Klein | Zendy; Lisa Dannenberg | Zendy; Tillman Lahres | Zendy; Lukas Clasen | Zendy; Klaus G. Schmidt | Zendy; Zhaoping Ding | Zendy; Birgit Donner | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Pannexin-1 Deficient Mice Have an Increased Susceptibility for Atrial Fibrillation and Show a QT-Prolongation Phenotype

Author(s) -

Stella Petric,

Sofia Klein,

Lisa Dannenberg,

Tillman Lahres,

Lukas Clasen,

Klaus G. Schmidt,

Zhaoping Ding,

Birgit Donner

Publication year - 2016

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000438645

Subject(s) - qt interval , cardiac electrophysiology , intracardiac injection , atrial fibrillation , pannexin , medicine , cardiology , electrophysiology , herg , context (archaeology) , stimulation , potassium channel , gap junction , biology , connexin , microbiology and biotechnology , paleontology , intracellular

Pannexin-1 (Panx1) is an ATP release channel that is ubiquitously expressed and coupled to several ligand-gated receptors. In isolated cardiac myocytes, Panx1 forms large conductance channels that can be activated by Ca2+ release from the sarcoplasmic reticulum. Here we characterized the electrophysiological function of these channels in the heart in vivo, taking recourse to mice with Panx1 ablation.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research