Exposure of Pancreatic β-Cells to Excess Glucose Results in Bimodal Activation of mTORC1 and mTOR-Dependent Metabolic Acceleration
Author:
Funder
NIH
Vanderbilt University Medical Center
Vanderbilt Diabetes Research and Training Center
Publisher
Elsevier BV
Subject
Multidisciplinary
Reference35 articles.
1. Overexpression of kinase-dead mTOR impairs glucose homeostasis by regulating insulin secretion and not beta-cell mass;Alejandro;Diabetes,2017
2. mTORC1 signaling: a double-edged sword in diabetic beta cells;Ardestani;Cell Metab.,2018
3. mTORC1 signaling and the metabolic control of cell growth;Ben-Sahra;Curr. Opin. Cell Biol.,2017
4. Loss of mTORC1 signalling impairs beta-cell homeostasis and insulin processing;Blandino-Rosano;Nat. Commun.,2017
5. The dynamic plasticity of insulin production in beta-cells;Boland;Mol. Metab.,2017
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