Ontology highlight
ABSTRACT: Rationale
Shortly after birth, muscle cells of the mammalian heart lose their ability to divide. Thus, they are unable to effectively replace dying cells in the injured heart. The recent discovery that the transcriptional coactivator Yes-associated protein (Yap) is necessary and sufficient for cardiomyocyte proliferation has gained considerable attention. However, the upstream regulators and signaling pathways that control Yap activity in the heart are poorly understood.Objective
To investigate the role of α-catenins in the heart using cardiac-specific αE- and αT-catenin double knockout mice.Methods and results
We used 2 cardiac-specific Cre transgenes to delete both αE-catenin (Ctnna1) and αT-catenin (Ctnna3) genes either in the perinatal or in the adult heart. Per
SUBMITTER: Li J
PROVIDER: S-EPMC4282606 | biostudies-literature | 2015 Jan
REPOSITORIES: biostudies-literature