Mitochondria control store‐operated Ca2+ entry through Na+ and redox signals
Tsipi Ben-Kasus Nissim(Ben-Gurion University of the Negev), Israel Sekler(Ben-Gurion University of the Negev), Yandong Zhou(Pennsylvania State University), Michal Hershfinkel(Ben-Gurion University of the Negev), Judith A. Stolwijk(University Hospital Regensburg), Mohamed Trebak(Historical Society of Western Pennsylvania), Xuexin Zhang(Harbin Medical University), Assaf Elazar(Ben-Gurion University of the Negev), Maxime Guéguinou(Université de Tours), Rajender K. Motiani(Regional Centre for Biotechnology), Donald L. Gill(Penn State Milton S. Hershey Medical Center), Soumitra Roy(Ben-Gurion University of the Negev), Nadine Hempel(University of Pittsburgh)
Cited by 105
Related Papers
NCLX is an essential component of mitochondrial Na <sup>+</sup> /Ca <sup>2+</sup> exchange
|Proceedings of the National Academy of Sciences|2009|776
Zinc in the physiology and pathology of the CNS
|Nature reviews. Neuroscience|2009|759
The Calcium Store Sensor, STIM1, Reciprocally Controls Orai and Ca <sub>V</sub> 1.2 Channels
|Science|2010|334
A zinc-sensing receptor triggers the release of intracellular Ca <sup>2+</sup> and regulates ion transport
|Proceedings of the National Academy of Sciences|2001|257
Synaptically Released Zinc Triggers Metabotropic Signaling via a Zinc-Sensing Receptor in the Hippocampus
|Journal of Neuroscience|2009|229