| First Author | Mao J | Year | 2008 |
| Journal | J Cell Biochem | Volume | 105 |
| Issue | 4 | Pages | 1073-80 |
| PubMed ID | 18777517 | Mgi Jnum | J:309934 |
| Mgi Id | MGI:6708993 | Doi | 10.1002/jcb.21910 |
| Citation | Mao J, et al. (2008) Drak2 overexpression results in increased beta-cell apoptosis after free fatty acid stimulation. J Cell Biochem 105(4):1073-80 |
| abstractText | Drak2 is a serine threonine kinase in the death-associated protein family. In this study, we investigated its role in free fatty acid (FFA)-induced islet apoptosis. Drak2 mRNA and protein were rapidly induced in islet beta-cells after FFA stimulation. Such Drak2 upregulation was accompanied by increased beta-cell apoptosis, which was inhibited by Drak2 knockdown using siRNA. Conversely, transgenic (Tg) Drak2 overexpression led to aggravated beta-cell apoptosis triggered by FFA. Drak2 overexpression in islets compromised the increase of anti-apoptotic factors, such as Bcl-2, Bcl-xL and Flip, upon FFA assault. Further in vivo experiments demonstrated that Drak2 Tg mice presented compromised glucose tolerance in a diet-induced obesity model. Our data show that Drak2 is detrimental to islet survival in the presence of excessive lipid. |
