Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.

doi:10.1093/cvr/cvv235

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Article

Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.

Cardiovascular research - 1 Dec 2015

Keller Kirsten, Maass Martina, Dizayee Sara, Leiss Veronika, Annala Suvi, Köth Jessica, Seemann Wiebke K, Müller-Ehmsen Jochen, Mohr Klaus, Nürnberg Bernd, Engelhardt Stefan, Herzig Stefan, Birnbaumer Lutz, Matthes Jan

Abstract excerpt

AIMS: Inhibitory G (Gi) proteins have been proposed to be cardioprotective. We investigated effects of Gαi2 knockout on cardiac function and survival in a murine heart failure model of cardiac β1-adrenoceptor overexpression. METHODS AND RESULTS: β1-transgenic mice lacking Gαi2 (β1-tg/Gαi2 (-/-)) were compared with wild-type mice and littermates either overexpressing cardiac β1-adrenoceptors (β1-tg) or lacking...

Topics

Animals
Atrial Natriuretic Factor
Cardiomyopathy, Dilated
Cyclic AMP
Cyclic AMP-Dependent Protein Kinases
Disease Models, Animal
GTP-Binding Protein alpha Subunit, Gi2
GTP-Binding Protein alpha Subunits, Gi-Go

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Gene Expression Regulation

Genetic Predisposition to Disease

Heart Failure

Mice, 129 Strain

Mice, Inbred C57BL

Mice, Knockout

Myocytes, Cardiac

Natriuretic Peptide, Brain

Phenotype

Receptors, Adrenergic, beta-1

Source

Open in PubMed Open full text

Identifiers

PMID: 26464333
DOI: 10.1093/cvr/cvv235
PMCID: PMC4648201

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

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