A murine model of neonatal diabetes mellitus in Glis3-deficient mice

被引：62

作者：

Watanabe, Naoki ^{[1
,2
]}

Hiramatsu, Kentaro ^{[1
,2
]}

Miyamoto, Rieko ^{[1
,2
]}

Yasuda, Kaoru ^{[3
]}

Suzuki, Norihiko ^{[3
]}

Oshima, Naoko ^{[4
]}

Kiyonari, Hiroshi ^{[4
]}

Shiba, Dai ^{[5
]}

Nishio, Saori ^{[6
]}

Mochizuki, Toshio ^{[6
]}

Yokoyama, Takahiko ^{[5
]}

Maruyama, Shoichi ^{[3
]}

Matsuo, Seiichi ^{[3
]}

Wakamatsu, Yuko ^{[1
,2
]}

Hashimoto, Hisashi ^{[1
,2
]}

机构：

[1] Nagoya Univ, Biosci & Biotechnol Ctr, Chikusa Ku, Nagoya, Aichi 4648601, Japan

[2] Nagoya Univ, Grad Sch Sci, Chikusa Ku, Nagoya, Aichi 4648601, Japan

[3] Nagoya Univ, Grad Sch Med, Nagoya, Aichi 4668550, Japan

[4] RIKEN, Ctr Dev Biol, Lab Anim Resources & Genet Engn, Kobe, Hyogo 6500047, Japan

[5] Kyoto Prefecture Univ Med, Dept Anat & Dev Biol, Kyoto 6020841, Japan

[6] Hokkaido Univ, Grad Sch Med, Dept Med 2, Sapporo, Hokkaido 0608638, Japan

来源：

FEBS LETTERS | 2009年 / 583卷 / 12期

关键词：

Diabetes; PKD; POLYCYSTIC KIDNEY-DISEASE; ZINC-FINGER PROTEIN; CONGENITAL HYPOTHYROIDISM; TRANSCRIPTION FACTOR; REPRESSOR FUNCTIONS; PANCREAS; GLIS3; CELL; TRANSACTIVATION; DIFFERENTIATION;

D O I：

10.1016/j.febslet.2009.05.039

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：2108 / 2113

页数：6

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