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Stabilised beta-catenin in postnatal ventricular myocardium leads to dilated cardiomyopathy and premature death.

Authors: Hirschy, Alain  Croquelois, Adrien  Perriard, Evelyne  Schoenauer, Roman  Agarkova, Irina  Hoerstrup, Simon P  Taketo, Makoto M  Pedrazzini, Thierry  Perriard, Jean-Claude  Ehler, Elisabeth 
Citation: Hirschy A, etal., Basic Res Cardiol. 2010 Sep;105(5):597-608. doi: 10.1007/s00395-010-0101-8. Epub 2010 Apr 8.
Pubmed: (View Article at PubMed) PMID:20376467
DOI: Full-text: DOI:10.1007/s00395-010-0101-8

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.


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CRRD Object Information
CRRD ID: 13524857
Created: 2018-04-30
Species: All species
Last Modified: 2018-04-30
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.