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10.1016/j.bbamcr.2014.03.022

http://scihub22266oqcxt.onion/10.1016/j.bbamcr.2014.03.022
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C4285153!4285153!24690484
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suck abstract from ncbi


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pmid24690484      Biochim+Biophys+Acta 2014 ; 1843 (10): 2233-9
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  • Calcium trafficking integrates endoplasmic reticulum function with mitochondrial bioenergetics #MMPMID24690484
  • Kaufman RJ; Malhotra JD
  • Biochim Biophys Acta 2014[Oct]; 1843 (10): 2233-9 PMID24690484show ga
  • Calcium homeostasis is central to all cellular functions and has been studied for decades. Calcium acts as a critical second messenger for both extracellular and intracellular signaling and is fundamental in cell life and death decisions [1]. The calcium gradient in the cell is coupled with an inherent ability of the divalent cation to reversibly bind multiple target biological molecules to generate an extremely versatile signaling system [2]. Calcium signals are used by the cell to control diverse processes as development, neurotransmitter release, muscle contraction, metabolism, autophagy and cell death. ?Cellular calcium overload? is detrimental to cellular health, resulting in massive activation of proteases and phospholipases leading to cell death [3]. Historically, cell death associated with calcium ion perturbations has been primarily recognized as necrosis. Recent evidence clearly associate changes in calcium ion concentrations with more sophisticated forms of cellular demise, including apoptosis [4] [5] [6] [7]. Although the endoplasmic reticulum (ER) serves as the primary calcium store in the metazoan cell, dynamic calcium release to the cytosol, mitochondria, nuclei and other organelles orchestrate diverse coordinated responses. Most evidence supports that calcium transport from the ER to mitochondria plays a significant role in regulating cellular bioenergetics, production of reactive oxygen species, induction of autophagy and apoptosis. Recently, molecular identities that mediate calcium traffic between the ER and mitochondria have been discovered [8] [9] [10]. The next questions are how they are regulated for exquisite tight control of ER ? mitochondrial calcium dynamics. This review attempts to summarize recent advances in the role of calcium in regulation of ER and mitochondrial function.
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