ERK1 is dispensable for mouse pancreatic beta cell function but is necessary for glucose-induced full activation of MSK1 and CREB

Abstract : Insufficient insulin secretion from pancreatic beta cells, which is associated with a decrease in beta cell mass, is a characteristic of type 2 diabetes. Extracellular signal-related kinase 1 and 2 (ERK1/2) inhibition in beta cells has been reported to affect insulin secretion, gene transcription and survival, although whether ERK1 and ERK2 play distinct roles is unknown. The aim of this study was to assess the individual roles of ERK1 and ERK2 in beta cells using ERK1 (also known as Mapk3)-knockout mice (Erk1 -/- mice) and pharmacological approaches.
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https://hal.umontpellier.fr/hal-02073008
Contributeur : Sandrine Beraud <>
Soumis le : mardi 19 mars 2019 - 15:29:04
Dernière modification le : samedi 10 août 2019 - 01:17:10

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Michèle Leduc, Joy Richard, Safia Costes, Dany Muller, Annie Varrault, et al.. ERK1 is dispensable for mouse pancreatic beta cell function but is necessary for glucose-induced full activation of MSK1 and CREB. Diabetologia, Springer Verlag, 2017, 60 (10), pp.1999-2010. ⟨10.1007/s00125-017-4356-6⟩. ⟨hal-02073008⟩

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