| First Author | Watanabe N | Year | 2009 |
| Journal | FEBS Lett | Volume | 583 |
| Issue | 12 | Pages | 2108-13 |
| PubMed ID | 19481545 | Mgi Jnum | J:150077 |
| Mgi Id | MGI:3849651 | Doi | 10.1016/j.febslet.2009.05.039 |
| Citation | Watanabe N, et al. (2009) A murine model of neonatal diabetes mellitus in Glis3-deficient mice. FEBS Lett 583(12):2108-13 |
| abstractText | Glis3 is a member of the Gli-similar subfamily. GLIS3 mutations in humans lead to neonatal diabetes, hypothyroidism, and cystic kidney disease. We generated Glis3-deficient mice by gene-targeting. The Glis3(-/-) mice had significant increases in the basal blood sugar level during the first few days after birth. The high levels of blood sugar are attributed to a decrease in the Insulin mRNA level in the pancreas that is caused by impaired islet development and the subsequent impairment of Insulin-producing cell formation. The pancreatic phenotypes indicate that the Glis3-deficient mice are a model for GLIS3 mutation and diabetes mellitus in humans. |
