| Literature DB >> 19481545 |
Naoki Watanabe1, Kentaro Hiramatsu, Rieko Miyamoto, Kaoru Yasuda, Norihiko Suzuki, Naoko Oshima, Hiroshi Kiyonari, Dai Shiba, Saori Nishio, Toshio Mochizuki, Takahiko Yokoyama, Shoichi Maruyama, Seiichi Matsuo, Yuko Wakamatsu, Hisashi Hashimoto.
Abstract
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.Entities:
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Year: 2009 PMID： 19481545 DOI： 10.1016/j.febslet.2009.05.039
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124