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ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally
Authors:Jean-Paul Decuypere  Jan B Parys  Geert Bultynck
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
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.
Keywords:autophagic flux  autophagy  Ca2+ microdomains  Ca2+ signaling  inositol 1  4  5-trisphosphate receptor  spatio-temporal Ca2+ signals
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