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ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally

ITPRs (inositol 1,4,5-trisphosphate receptors), the main endoplasmic reticulum (ER) Ca(2+)-release channels, were originally proposed as suppressors of autophagy. Yet, new evidence has accumulated over recent years supporting a crucial, stimulatory role for ITPRs in driving the autophagic flux. Here...

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Detalles Bibliográficos
Autores principales: Decuypere, Jean-Paul, Parys, Jan B, Bultynck, Geert
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824608/
https://www.ncbi.nlm.nih.gov/pubmed/26291777
http://dx.doi.org/10.1080/15548627.2015.1083666
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author Decuypere, Jean-Paul
Parys, Jan B
Bultynck, Geert
author_facet Decuypere, Jean-Paul
Parys, Jan B
Bultynck, Geert
author_sort Decuypere, Jean-Paul
collection PubMed
description ITPRs (inositol 1,4,5-trisphosphate receptors), the main endoplasmic reticulum (ER) Ca(2+)-release channels, were originally proposed as suppressors of autophagy. Yet, new evidence has accumulated over recent years supporting a crucial, stimulatory role for ITPRs in driving the autophagic flux. Here, we provide an integrated view on how ITPR-mediated Ca(2+) signaling can have a dual impact on autophagy, depending on the characteristics of the spatio-temporal Ca(2+) signals, including the existence of ER-mitochondrial and ER-lysosomal Ca(2+) signaling microdomains.
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spelling pubmed-48246082016-04-27 ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally Decuypere, Jean-Paul Parys, Jan B Bultynck, Geert Autophagy Views and Commentaries ITPRs (inositol 1,4,5-trisphosphate receptors), the main endoplasmic reticulum (ER) Ca(2+)-release channels, were originally proposed as suppressors of autophagy. Yet, new evidence has accumulated over recent years supporting a crucial, stimulatory role for ITPRs in driving the autophagic flux. Here, we provide an integrated view on how ITPR-mediated Ca(2+) signaling can have a dual impact on autophagy, depending on the characteristics of the spatio-temporal Ca(2+) signals, including the existence of ER-mitochondrial and ER-lysosomal Ca(2+) signaling microdomains. Taylor & Francis 2015-08-20 /pmc/articles/PMC4824608/ /pubmed/26291777 http://dx.doi.org/10.1080/15548627.2015.1083666 Text en © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Views and Commentaries
Decuypere, Jean-Paul
Parys, Jan B
Bultynck, Geert
ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
title ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
title_full ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
title_fullStr ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
title_full_unstemmed ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
title_short ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
title_sort itprs/inositol 1,4,5-trisphosphate receptors in autophagy: from enemy to ally
topic Views and Commentaries
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824608/
https://www.ncbi.nlm.nih.gov/pubmed/26291777
http://dx.doi.org/10.1080/15548627.2015.1083666
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