An inside job: Annexin 1A-Inositol 1,4,5-trisphosphate receptor interaction conveys endoplasmic reticulum luminal Ca2+ sensitivity |
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| Institution: | 1. Department of Cell and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK;2. Institute of Clinical Medicine, University of Oslo, 0318, Oslo, Norway;3. Department of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, 0310, Oslo, Norway;4. Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, 14186, Stockholm, Sweden;1. Institute of Neuroscience, Technical University Munich, Biedersteiner Str. 29, 80802, Munich, Germany;2. UK Dementia Research Institute at UCL, University College London, Gower Street, London, WC1E 6BT, United Kingdom;3. CNS Diseases Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany;4. Munich Cluster for Systems Neurology (SyNergy), Biedersteiner Str. 29, 80802, Munich, Germany;3. MitoCare Center, Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107;4. Department of Pharmacology & Physiology, University of Rochester, Rochester, New York 14642;5. Center for Perinatal Research, Research Institute, Nationwide Children''s Hospital, Columbus, Ohio 43205 |
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| Abstract: | Cytoplasmic Ca2+ is a pivotal regulator of IP3R activity. It is however controversial whether the Ca2+] in the Endoplasmic Reticulum lumen also directly regulates channel function. We highlight a recent paper that demonstrates that luminal Ca2+] potently inhibits IP3R activity. This regulation occurs indirectly by an interaction mediated through a binding partner, likely Annexin 1A. |
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| Keywords: | Inositol 1 4 5 trisphosphate receptor Annexin 1A Endoplasmic Reticulum |
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