| First Author | Ahlgren U | Year | 1998 |
| Journal | Genes Dev | Volume | 12 |
| Issue | 12 | Pages | 1763-8 |
| PubMed ID | 9637677 | Mgi Jnum | J:48516 |
| Mgi Id | MGI:1270086 | Doi | 10.1101/gad.12.12.1763 |
| Citation | Ahlgren U, et al. (1998) beta-cell-specific inactivation of the mouse Ipf1/Pdx1 gene results in loss of the beta-cell phenotype and maturity onset diabetes. Genes Dev 12(12):1763-8 |
| abstractText | To study the late beta-cell-specific function of the homeodomain protein IPF1/PDX1 we have generated mice in which the Ipf1/Pdx1 gene has been disrupted specifically in beta cells. These mice develop diabetes with age, and we show that IPF1/PDX1 is required for maintaining the beta cell identity by positively regulating insulin and islet amyloid polypeptide expression and by repressing glucagon expression. We also provide evidence that IPF1/PDX1 regulates the expression of Glut2 in a dosage- dependent manner suggesting that lowered IPF1/ PDX1 activity may contribute to the development of type II diabetes by causing impaired expression of both Glut2 and insulin. |
