beta-cell-specific inactivation of the mouse Ipf1/Pdx1 gene results in loss of the beta-cell phenotype and maturity onset diabetes.

作者: U. Ahlgren , J. Jonsson , L. Jonsson , K. Simu , H. Edlund

DOI: 10.1101/GAD.12.12.1763

关键词:

摘要: To study the late beta-cell-specific function of homeodomain protein IPF1/PDX1 we have generated mice in which Ipf1/Pdx1 gene has been disrupted specifically beta cells. These develop diabetes with age, and show that is required for maintaining cell identity by positively regulating insulin islet amyloid polypeptide expression repressing glucagon expression. We also provide evidence regulates Glut2 a dosage-dependent manner suggesting lowered activity may contribute to development type II causing impaired both insulin.

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