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• W2108929125 abstract "In pancreatic β cells, ERK1 and ERK2 participate in nutrient sensing, and their activities rise and fall as a function of glucose concentration over the physiologic range. Glucose metabolism triggers calcium influx and release of calcium from intracellular stores to activate ERK1/2. Calcium influx also activates the calcium-dependent phosphatase calcineurin, which is required for maximal ERK1/2 activation by glucose. Calcineurin controls insulin gene expression by ERK1/2-dependent and -independent mechanisms. Here, we show that, in β cells, glucose activates the ERK1/2 cascade primarily through B-Raf. Glucose activation of B-Raf, like that of ERK1/2, is calcineurin-sensitive. Calcineurin binds to B-Raf in both unstimulated and stimulated cells. We show that B-Raf is a calcineurin substrate; among calcineurin target residues on B-Raf is T401, a site of negative feedback phosphorylation by ERK1/2. Blocking calcineurin activity in β cells prevents dephosphorylation of B-Raf T401 and decreases B-Raf and ERK1/2 activities. We conclude that the major calcineurin-dependent event in glucose sensing by ERK1/2 is the activation of B-Raf." @default.
• W2108929125 created "2016-06-24" @default.
• W2108929125 creator A5013331146 @default.
• W2108929125 creator A5038141288 @default.
• W2108929125 date "2010-12-06" @default.
• W2108929125 modified "2023-10-17" @default.
• W2108929125 title "Calcineurin increases glucose activation of ERK1/2 by reversing negative feedback" @default.
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• W2108929125 doi "https://doi.org/10.1073/pnas.1016630108" @default.
• W2108929125 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3009760" @default.
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• W2108929125 hasPublicationYear "2010" @default.
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