Nupr1 deletion protects against glucose intolerance by increasing beta cell mass

Aims/hypothesis The stress-activated nuclear protein transcription regulator 1 (NUPR1) is induced in response to glucose and TNF-α, both of which are elevated in type 2 diabetes, and Nupr1 has been implicated in cell proliferation and apoptosis cascades. We used Nupr1 −/− mice to study the role of N...

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Veröffentlicht in:	Diabetologia 2013-11, Vol.56 (11), p.2477-2486
Hauptverfasser:	Barbosa-Sampaio, Helena C., Liu, Bo, Drynda, Robert, Rodriguez de Ledesma, Ana M., King, Aileen J., Bowe, James E., Malicet, Cédric, Iovanna, Juan L., Jones, Peter M., Persaud, Shanta J., Muller, Dany S.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antibodies Apoptosis Biological and medical sciences Blotting, Western Cell cycle Cell growth Diabetes Diabetes. Impaired glucose tolerance DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gene expression Glucagon Glucose Glucose Intolerance - genetics Glucose Intolerance - metabolism Homeostasis Human Physiology Humans Immunohistochemistry Insulin resistance Insulin-Secreting Cells - cytology Insulin-Secreting Cells - metabolism Internal Medicine Male Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolism Mice Mice, Knockout Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Pancreas Proteins Transcription factors
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