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Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway
Functional intracellular Ca(2+) signaling is essential for the upregulation of the canonical mTOR-controlled autophagy pathway triggered by rapamycin or by nutrient deprivation. Moreover, modifications in the Ca(2+)-signaling machinery coincide with autophagy stimulation. This results in enhanced in...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829968/ https://www.ncbi.nlm.nih.gov/pubmed/24265855 http://dx.doi.org/10.4161/cib.25429 |
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author | Decuypere, Jean-Paul Paudel, Ram Chandra Parys, Jan Bultynck, Geert |
author_facet | Decuypere, Jean-Paul Paudel, Ram Chandra Parys, Jan Bultynck, Geert |
author_sort | Decuypere, Jean-Paul |
collection | PubMed |
description | Functional intracellular Ca(2+) signaling is essential for the upregulation of the canonical mTOR-controlled autophagy pathway triggered by rapamycin or by nutrient deprivation. Moreover, modifications in the Ca(2+)-signaling machinery coincide with autophagy stimulation. This results in enhanced intracellular Ca(2+) signaling essential for driving the autophagy process. Yet, the mechanisms upstream (the players causing the changes in Ca(2+) signaling) and downstream (the targets of the altered Ca(2+) signals) of this Ca(2+)-dependent autophagy pathway remain elusive. Here, we speculate about these mechanisms based on our current knowledge. |
format | Online Article Text |
id | pubmed-3829968 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-38299682013-11-21 Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway Decuypere, Jean-Paul Paudel, Ram Chandra Parys, Jan Bultynck, Geert Commun Integr Biol Short Communication Functional intracellular Ca(2+) signaling is essential for the upregulation of the canonical mTOR-controlled autophagy pathway triggered by rapamycin or by nutrient deprivation. Moreover, modifications in the Ca(2+)-signaling machinery coincide with autophagy stimulation. This results in enhanced intracellular Ca(2+) signaling essential for driving the autophagy process. Yet, the mechanisms upstream (the players causing the changes in Ca(2+) signaling) and downstream (the targets of the altered Ca(2+) signals) of this Ca(2+)-dependent autophagy pathway remain elusive. Here, we speculate about these mechanisms based on our current knowledge. Landes Bioscience 2013-09-01 2013-06-25 /pmc/articles/PMC3829968/ /pubmed/24265855 http://dx.doi.org/10.4161/cib.25429 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Short Communication Decuypere, Jean-Paul Paudel, Ram Chandra Parys, Jan Bultynck, Geert Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway |
title | Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway |
title_full | Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway |
title_fullStr | Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway |
title_full_unstemmed | Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway |
title_short | Intracellular Ca(2+) signaling: A novel player in the canonical mTOR-controlled autophagy pathway |
title_sort | intracellular ca(2+) signaling: a novel player in the canonical mtor-controlled autophagy pathway |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829968/ https://www.ncbi.nlm.nih.gov/pubmed/24265855 http://dx.doi.org/10.4161/cib.25429 |
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