期刊
FEBS LETTERS
卷 583, 期 12, 页码 2108-2113出版社
WILEY
DOI: 10.1016/j.febslet.2009.05.039
关键词
Diabetes; PKD
资金
- Ministry of Education, Science, Sports, Culture, and Technology
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. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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