Calcium at the Center of Cell Signaling: Interplay between Endoplasmic Reticulum, Mitochondria, and Lysosomes
In recent years, rapid discoveries have been made relating to Ca2+ handling at specific organelles that have important implications for whole-cell Ca2+ homeostasis. In particular, the structures of the endoplasmic reticulum (ER) Ca2+ channels revealed by electron cryomicroscopy (cryo-EM), continuous...
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| Published in: | Trends in biochemical sciences (Amsterdam. Regular ed.) Vol. 41; no. 12; pp. 1035 - 1049 |
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| Main Authors: | , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
England
Elsevier Ltd
01.12.2016
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| Subjects: | |
| ISSN: | 0968-0004, 1362-4326 |
| Online Access: | Get full text |
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| Summary: | In recent years, rapid discoveries have been made relating to Ca2+ handling at specific organelles that have important implications for whole-cell Ca2+ homeostasis. In particular, the structures of the endoplasmic reticulum (ER) Ca2+ channels revealed by electron cryomicroscopy (cryo-EM), continuous updates on the structure, regulation, and role of the mitochondrial calcium uniporter (MCU) complex, and the analysis of lysosomal Ca2+ signaling are milestones on the route towards a deeper comprehension of the complexity of global Ca2+ signaling. In this review we summarize recent discoveries on the regulation of interorganellar Ca2+ homeostasis and its role in pathophysiology.
Ca2+ signaling is regulated by the intimate interconnection between intracellular organelles and plasma membrane channels.
The ultrastructures of endoplasmic reticulum and mitochondrial Ca2+ channels have been determined.
Great advances have been made in our understanding of the function and regulation of the mitochondrial calcium uniporter.
Studies on endolysosomal Ca2+ signaling unravel a potential contribution of this compartment to global Ca2+ homeostasis. |
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| Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
| ISSN: | 0968-0004 1362-4326 |
| DOI: | 10.1016/j.tibs.2016.09.001 |