| First Author | White DE | Year | 2006 |
| Journal | Genes Dev | Volume | 20 |
| Issue | 17 | Pages | 2355-60 |
| PubMed ID | 16951252 | Mgi Jnum | J:112174 |
| Mgi Id | MGI:3655759 | Doi | 10.1101/gad.1458906 |
| Citation | White DE, et al. (2006) Targeted ablation of ILK from the murine heart results in dilated cardiomyopathy and spontaneous heart failure. Genes Dev 20(17):2355-60 |
| abstractText | A requirement for integrin-mediated adhesion in cardiac physiology is revealed through targeted deletion of integrin-associated genes in the murine heart. Here we show that targeted ablation of the integrin-linked kinase (ILK) expression results in spontaneous cardiomyopathy and heart failure by 6 wk of age. Deletion of ILK results in disaggregation of cardiomyocytes, associated with disruption of adhesion signaling through the beta1-integrin/FAK (focal adhesion kinase) complex. Importantly, the loss of ILK is accompanied by a reduction in cardiac Akt phosphorylation, which normally provides a protective response against stress. Together, these results suggest that ILK plays a central role in protecting the mammalian heart against cardiomyopathy and failure. |
