Ribosome-free Terminals of Rough ER Allow Formation of STIM1 Puncta and Segregation of STIM1 from IP3 Receptors
Open Access
- 13 October 2009
- journal article
- research article
- Published by Elsevier BV in Current Biology
- Vol. 19 (19), 1648-1653
- https://doi.org/10.1016/j.cub.2009.07.072
Abstract
No abstract availableKeywords
This publication has 32 references indexed in Scilit:
- STIM1 Clusters and Activates CRAC Channels via Direct Binding of a Cytosolic Domain to Orai1Cell, 2009
- SOAR and the polybasic STIM1 domains gate and regulate Orai channelsNature, 2009
- ATP depletion induces translocation of STIM1 to puncta and formation of STIM1–ORAI1 clusters: translocation and re-translocation of STIM1 does not require ATPPflügers Archiv - European Journal of Physiology, 2008
- STIM2 Is a Feedback Regulator that Stabilizes Basal Cytosolic and Endoplasmic Reticulum Ca2+ LevelsCell, 2007
- Visualization and Manipulation of Plasma Membrane-Endoplasmic Reticulum Contact Sites Indicates the Presence of Additional Molecular Components within the STIM1-Orai1 ComplexJournal of Biological Chemistry, 2007
- Recent breakthroughs in the molecular mechanism of capacitative calcium entry (with thoughts on how we got here)Cell Calcium, 2007
- The elementary unit of store-operated Ca2+ entry: local activation of CRAC channels by STIM1 at ER–plasma membrane junctionsThe Journal of cell biology, 2006
- Ca2+ store depletion causes STIM1 to accumulate in ER regions closely associated with the plasma membraneThe Journal of cell biology, 2006
- A mutation in Orai1 causes immune deficiency by abrogating CRAC channel functionNature, 2006
- STIM Is a Ca2+ Sensor Essential for Ca2+-Store-Depletion-Triggered Ca2+ InfluxCurrent Biology, 2005