Gαq and Gα11 contribute to the maintenance of cellular electrophysiology and Ca2+ handling in ventricular cardiomyocytes | Zendy

Sara Pahlavan | Zendy; Martin Oberhofer | Zendy; Benjamin Sauer | Zendy; Sandra Ruppenthal | Zendy; Xiao Yu Tian | Zendy; Anke Scholz | Zendy; Lars Kaestner | Zendy; Peter Lipp | Zendy

Open Access

Gαq and Gα11 contribute to the maintenance of cellular electrophysiology and Ca2+ handling in ventricular cardiomyocytes

Author(s) -

Sara Pahlavan,

Martin Oberhofer,

Benjamin Sauer,

Sandra Ruppenthal,

Xiao Yu Tian,

Anke Scholz,

Lars Kaestner,

Peter Lipp

Publication year - 2012

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvs162

Subject(s) - myocyte , medicine , electrophysiology , basal (medicine) , cardiac myocyte , cardiology , cardiac electrophysiology , muscle hypertrophy , cardiac hypertrophy , atrial myocytes , endocrinology , biology , insulin

Gα(q) and Gα(11) signalling pathways contribute to cardiac diseases such as hypertrophy and arrhythmia, but their role in cardiac myocytes from healthy hearts has remained unclear. We aimed to investigate the contribution of Gα(q) and Gα(11) signalling to the basal properties of ventricular myocytes.

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