ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally |
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Authors: | Jean-Paul Decuypere Jan B Parys Geert Bultynck |
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Institution: | 1.KU Leuven Department of Microbiology and Immunology, Laboratory of Abdominal Transplantation; University Hospitals Leuven Department of Abdominal Transplant Surgery; Leuven, Belgium;2.KU Leuven Department of Cellular and Molecular Medicine, Laboratory of Molecular and Cellular Signaling; Leuven, Belgium |
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Abstract: | ITPRs (inositol 1,4,5-trisphosphate receptors), the main endoplasmic reticulum (ER) Ca2+-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 Ca2+ signaling can have a dual impact on autophagy, depending on the characteristics of the spatio-temporal Ca2+ signals, including the existence of ER-mitochondrial and ER-lysosomal Ca2+ signaling microdomains. |
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Keywords: | autophagic flux autophagy Ca2+ microdomains Ca2+ signaling inositol 1 4 5-trisphosphate receptor spatio-temporal Ca2+ signals |
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