| First Author | Chang Z | Year | 2010 |
| Journal | Dev Biol | Volume | 347 |
| Issue | 2 | Pages | 384-91 |
| PubMed ID | 20816796 | Mgi Jnum | J:166615 |
| Mgi Id | MGI:4848252 | Doi | 10.1016/j.ydbio.2010.08.033 |
| Citation | Chang Z, et al. (2010) Deletion of Akt1 causes heart defects and abnormal cardiomyocyte proliferation. Dev Biol 347(2):384-91 |
| abstractText | The PI3K-PDK1-PKB/Akt (PI3K, phosphoinositide-3 kinase; PDK1, phosphoinositide-dependent protein kinase 1; PKB, protein kinase B) signaling pathway plays a critical role in a variety of biological processes including cell survival, growth and proliferation, metabolism and organogenesis. Previously, we generated Akt1-deficient mice and found high neonatal mortality with unknown causes. Here we report that histological analysis of Akt1-deficient embryos and newborns revealed heart defects and decreased cell proliferation. Echocardiographic study of Akt1-deficient mice indicated decreased heart function. Further investigation revealed that Akt1 deficiency caused substantial activation of p38MAPK in the heart. Breeding the Akt1-deficient mice to mice that were heterozygous for a null p38alpha partially rescued the heart defects, significantly decreased post-natal mortality, and restored normal patterns of cardiomyocyte proliferation. Our study suggests that Akt1 is essential for heart development and function, in part, through suppression of p38MAPK activation. |
