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Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell

The Mitochondrial Calcium Uniporter Complex (MCU Complex) is essential for β-cell function due to its role in sustaining insulin secretion. The MCU complex regulates mitochondrial Ca(2+) influx, which is necessary for increased ATP production following cellular glucose uptake, keeps the cell membran...

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Detalles Bibliográficos
Autores principales: Allen, Jack G., Tessem, Jeffery S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265474/
https://www.ncbi.nlm.nih.gov/pubmed/35805078
http://dx.doi.org/10.3390/cells11131993
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author Allen, Jack G.
Tessem, Jeffery S.
author_facet Allen, Jack G.
Tessem, Jeffery S.
author_sort Allen, Jack G.
collection PubMed
description The Mitochondrial Calcium Uniporter Complex (MCU Complex) is essential for β-cell function due to its role in sustaining insulin secretion. The MCU complex regulates mitochondrial Ca(2+) influx, which is necessary for increased ATP production following cellular glucose uptake, keeps the cell membrane K(+) channels closed following initial insulin release, and ultimately results in sustained insulin granule exocytosis. Dysfunction in Ca(2+) regulation results in an inability to sustain insulin secretion. This review defines the functions, structure, and mutations associated with the MCU complex members mitochondrial calcium uniporter protein (MCU), essential MCU regulator (EMRE), mitochondrial calcium uptake 1 (MICU1), mitochondrial calcium uptake 2 (MICU2), and mitochondrial calcium uptake 3 (MICU3) in the pancreatic β-cell. This review provides a framework for further evaluation of the MCU complex in β-cell function and insulin secretion.
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spelling pubmed-92654742022-07-09 Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell Allen, Jack G. Tessem, Jeffery S. Cells Review The Mitochondrial Calcium Uniporter Complex (MCU Complex) is essential for β-cell function due to its role in sustaining insulin secretion. The MCU complex regulates mitochondrial Ca(2+) influx, which is necessary for increased ATP production following cellular glucose uptake, keeps the cell membrane K(+) channels closed following initial insulin release, and ultimately results in sustained insulin granule exocytosis. Dysfunction in Ca(2+) regulation results in an inability to sustain insulin secretion. This review defines the functions, structure, and mutations associated with the MCU complex members mitochondrial calcium uniporter protein (MCU), essential MCU regulator (EMRE), mitochondrial calcium uptake 1 (MICU1), mitochondrial calcium uptake 2 (MICU2), and mitochondrial calcium uptake 3 (MICU3) in the pancreatic β-cell. This review provides a framework for further evaluation of the MCU complex in β-cell function and insulin secretion. MDPI 2022-06-22 /pmc/articles/PMC9265474/ /pubmed/35805078 http://dx.doi.org/10.3390/cells11131993 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Allen, Jack G.
Tessem, Jeffery S.
Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell
title Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell
title_full Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell
title_fullStr Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell
title_full_unstemmed Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell
title_short Ca(2+) Sensors Assemble: Function of the MCU Complex in the Pancreatic Beta Cell
title_sort ca(2+) sensors assemble: function of the mcu complex in the pancreatic beta cell
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265474/
https://www.ncbi.nlm.nih.gov/pubmed/35805078
http://dx.doi.org/10.3390/cells11131993
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