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Stabilised beta-catenin in postnatal ventricular myocardium leads to dilated cardiomyopathy and premature death.
Basic Research in Cardiology
Beta-catenin is a component of the intercalated disc in cardiomyocytes, but can also be involved in signalling and activation of gene transcription. We wanted to determine how long-term changes in beta-catenin expression levels would affect mature cardiomyocytes. Conditional transgenic mice that either lacked beta-catenin or that expressed a non-degradable form of beta-catenin in the adult ventricle were created. While mice lacking beta-catenin in the ventricle do not have an overt phenotype, mice expressing a non-degradable form develop dilated cardiomyopathy and do not survive beyond 5 months. A detailed analysis could reveal that this phenotype is correlated with a distinct localisation of beta-catenin in adult cardiomyocytes, which cannot be detected in the nucleus, no matter how much protein is present. Our report is the first study that addresses long-term effects of either the absence of beta-catenin or its stabilisation on ventricular cardiomyocytes and it suggests that beta-catenin's role in the nucleus may be of little significance in the healthy adult heart.
myocyte-specific excision, cardiac-hypertrophy, intercalated disc, signaling pathway, mouse development, nuclear-membrane, progenitor cells, protein emerin, cancer cells, gene, Beta-catenin, Hypertrophy, Intercalated disc, Canonical Wnt signalling, Dilated cardiomyopathy
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