| First Author | Matus M | Year | 2007 |
| Journal | FASEB J | Volume | 21 |
| Issue | 8 | Pages | 1884-92 |
| PubMed ID | 17307839 | Mgi Jnum | J:134856 |
| Mgi Id | MGI:3789887 | Doi | 10.1096/fj.06-7915com |
| Citation | Matus M, et al. (2007) Cardiomyocyte-specific inactivation of transcription factor CREB in mice. FASEB J 21(8):1884-92 |
| abstractText | The transcription factor cAMP response element (CRE)-binding protein (CREB, Creb1) plays a critical role in regulating gene expression in response to activation of the cAMP-dependent signaling pathway, which is implicated in the pathophysiology of heart failure. Using the Cre-loxP system, we generated mice with a cardiomyocyte-specific inactivation of CREB and studied in this model whether CREB is critical for cardiac function. CREB-deficient mice were viable and displayed neither changes in cardiac morphology nor alterations of basal or isoproterenol-stimulated left ventricular function in vivo or of important cardiac regulatory proteins. Since CREB was proposed as a negative regulator of cardiomyocyte apoptosis by enhancing the expression of the antiapoptotic protein Bcl-2, we analyzed the fragmentation of DNA, the activity of caspases 3/7 and the expression of Bcl-2 and did not observe any differences between CREB-deficient and CREB-normal hearts. Our results suggest that the presence of CREB is not critical for normal cardiac function in mice. |
