التفاصيل البيبلوغرافية
| العنوان: |
A murine model of neonatal diabetes mellitus in Glis3-deficient mice |
| المؤلفون: |
Watanabe, Naoki, Hiramatsu, Kentaro, Miyamoto, Rieko, Yasuda, Kaoru, Suzuki, Norihiko, Oshima, Naoko, Kiyonari, Hiroshi, Shiba, Dai, Nishio, Saori, Mochizuki, Toshio, Yokoyama, Takahiko, Maruyama, Shoichi, Matsuo, Seiichi, Wakamatsu, Yuko, Hashimoto, Hisashi |
| المصدر: |
FEBS Letters; Jun2009, Vol. 583 Issue 12, p2108-2113, 6p |
| مصطلحات موضوعية: |
DIABETES in children, NEONATAL diseases, ANIMAL models of diabetes, HYPOTHYROIDISM in children, GENETIC mutation, CYSTIC kidney disease, BLOOD sugar, GENE targeting, MESSENGER RNA |
| مستخلص: |
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. [Copyright &y& Elsevier] |
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| قاعدة البيانات: |
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