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

FEBS letters | Jun 18, 2009

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.

Pubmed ID: 19481545 RIS Download

Mesh terms: Animals | Animals, Newborn | Base Sequence | Blood Glucose | Carboxypeptidases A | DNA Primers | Diabetes Mellitus, Type 1 | Disease Models, Animal | Humans | Infant, Newborn | Insulin | Islets of Langerhans | Mice | Mice, Knockout | Mutation | Pancreas | RNA, Messenger | Repressor Proteins | Trans-Activators | Transcription Factors

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Mouse Genome Informatics (Data, Gene Annotation)

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