Abstract
Transient receptor potential channels, especially the members of the melastatin family (TRPM), participate in insulin secretion. Some of them are substrates for protein kinases, which are involved in several neurotransmitter, incretin and hormonal signaling cascades in β cells. The functional relationships between protein kinases and TRPM channels in systems of heterologous expression and native tissues rise issues about novel regulation pathways of pancreatic β-cell excitability. The aim of the present work is to review the evidences about phosphorylation of TRPM channels in β cells and to discuss the perspectives on insulin secretion.
Keywords: Pancreatic beta cells, Insulin, Phosphorylation, TRP channels, Insulin Secretion, Phosphorylation, GLUT, 2-adrenergic, Alzheimer disease , glucose-conditioned closure.
Current Diabetes Reviews
Title:TRPM Channels Phosphorylation as a Potential Bridge Between Old Signals and Novel Regulatory Mechanisms of Insulin Secretion
Volume: 9 Issue: 2
Author(s): Carlos Manlio Diaz-Garcia, Carmen Sanchez-Soto and Marcia Hiriart
Affiliation:
Keywords: Pancreatic beta cells, Insulin, Phosphorylation, TRP channels, Insulin Secretion, Phosphorylation, GLUT, 2-adrenergic, Alzheimer disease , glucose-conditioned closure.
Abstract: Transient receptor potential channels, especially the members of the melastatin family (TRPM), participate in insulin secretion. Some of them are substrates for protein kinases, which are involved in several neurotransmitter, incretin and hormonal signaling cascades in β cells. The functional relationships between protein kinases and TRPM channels in systems of heterologous expression and native tissues rise issues about novel regulation pathways of pancreatic β-cell excitability. The aim of the present work is to review the evidences about phosphorylation of TRPM channels in β cells and to discuss the perspectives on insulin secretion.
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Cite this article as:
Diaz-Garcia Manlio Carlos, Sanchez-Soto Carmen and Hiriart Marcia, TRPM Channels Phosphorylation as a Potential Bridge Between Old Signals and Novel Regulatory Mechanisms of Insulin Secretion, Current Diabetes Reviews 2013; 9 (2) . https://dx.doi.org/10.2174/1573399811309020003
DOI https://dx.doi.org/10.2174/1573399811309020003 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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