| First Author | Rodgers JT | Year | 2010 |
| Journal | Cell Metab | Volume | 11 |
| Issue | 1 | Pages | 23-34 |
| PubMed ID | 20074525 | Mgi Jnum | J:157003 |
| Mgi Id | MGI:4429735 | Doi | 10.1016/j.cmet.2009.11.006 |
| Citation | Rodgers JT, et al. (2010) Cdc2-like kinase 2 is an insulin-regulated suppressor of hepatic gluconeogenesis. Cell Metab 11(1):23-34 |
| abstractText | Dynamic regulation of insulin signaling and metabolic gene expression is critical to nutrient homeostasis; dysregulation of these pathways is widely implicated in insulin resistance and other disease states. Though the metabolic effects of insulin are well established, the components linking insulin signal transduction to a metabolic response are not as well understood. Here, we show that Cdc2-like kinase 2 (Clk2) is an insulin-regulated suppressor of hepatic gluconeogenesis and glucose output. Clk2 protein levels and kinase activity are induced as part of the hepatic refeeding response by the insulin/Akt pathway. Clk2 directly phosphorylates the SR domain on PGC-1alpha, resulting in repression of gluconeogenic gene expression and hepatic glucose output. In addition, Clk2 is downregulated in db/db mice, and reintroduction of Clk2 largely corrects glycemia. Thus, we have identified a role for and regulation of the Clk2 kinase as a component of hepatic insulin signaling and glucose metabolism. |
