| First Author | Cheng P | Year | 2011 |
| Journal | FEBS Lett | Volume | 585 |
| Issue | 21 | Pages | 3403-8 |
| PubMed ID | 22001208 | Mgi Jnum | J:177497 |
| Mgi Id | MGI:5295314 | Doi | 10.1016/j.febslet.2011.09.043 |
| Citation | Cheng P, et al. (2011) Menin prevents liver steatosis through co-activation of peroxisome proliferator-activated receptor alpha. FEBS Lett 585(21):3403-8 |
| abstractText | Fatty liver is strongly associated with metabolic syndrome. Here, we show that the impaired hepatic expression of menin, the product of the MEN1 (multiple endocrine neoplasia type 1) tumor suppressor gene, represents a common feature of several fatty liver mouse models. The liver specific ablation of MEN1 gene expression in healthy mice induced hepatic steatosis under high-fat dietary conditions. Moreover, overexpression of menin in livers of steatotic db/db mice reduced liver triglyceride accumulation. At the molecular level, we found that menin acts synergistically with the nuclear receptor PPARalpha to control gene expression of fatty acid oxidation. Collectively, these data suggest a crucial role for menin as an integrator of the complex transcriptional network controlling hepatic steatosis. STRUCTURED SUMMARY OF PROTEIN INTERACTIONS: Meninphysically interacts with PPAR alpha by anti tag coimmunoprecipitation (View Interaction: 1, 2). |
