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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Base Sequence
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Blood Glucose / metabolism
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Carboxypeptidases A / metabolism
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DNA Primers / genetics
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DNA-Binding Proteins
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Diabetes Mellitus, Type 1 / genetics*
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Diabetes Mellitus, Type 1 / metabolism*
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Diabetes Mellitus, Type 1 / pathology
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Disease Models, Animal
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Humans
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Infant, Newborn
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Insulin / genetics
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Islets of Langerhans / metabolism
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Islets of Langerhans / pathology
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Mice
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Mice, Knockout
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Mutation
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Pancreas / metabolism
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Pancreas / pathology
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Repressor Proteins / genetics
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Trans-Activators / deficiency*
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Trans-Activators / genetics
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Transcription Factors / deficiency
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Transcription Factors / genetics
Substances
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Blood Glucose
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DNA Primers
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DNA-Binding Proteins
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GLIS3 protein, human
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Glis3 protein, mouse
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Insulin
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RNA, Messenger
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Repressor Proteins
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Trans-Activators
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Transcription Factors
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Carboxypeptidases A