| First Author | Piven OO | Year | 2011 |
| Journal | Exp Biol Med (Maywood) | Volume | 236 |
| Issue | 7 | Pages | 816-22 |
| PubMed ID | 21680756 | Mgi Jnum | J:285860 |
| Mgi Id | MGI:6401017 | Doi | 10.1258/ebm.2011.010362 |
| Citation | Piven OO, et al. (2011) Requirement for N-cadherin-catenin complex in heart development. Exp Biol Med (Maywood) 236(7):816-22 |
| abstractText | Cell adhesion, mediated by N-cadherin, is critical for embryogenesis since N-cadherin-null embryos die during mid-gestation with multiple developmental defects. To investigate the role of N-cadherin in heart muscle development, N-cadherin was specifically deleted from myocardial cells in mice. The structural integrity of the myocardial cell wall was compromised in the N-cadherin mutant embryos, leading to a malformed heart and a delay in embryonic development. In contrast, cardiac-specific deletion of alphaE-catenin, found in adherens junctions, or beta-catenin, did not cause any morphological defects in the embryonic heart, presumably due to compensation by alphaT-catenin that is normally found in intercalated disks and gamma-catenin (plakoglobin), respectively. Embryos lacking beta-catenin in the heart also exhibited a cardiac defect, but only later in development resulting in partial lethality. These genetic studies underscore the importance of the N-cadherin/catenin complex in cardiogenesis. |
