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lüll Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling Smaili SS; Hsu YT; Carvalho AC; Rosenstock TR; Sharpe JC; Youle RJBraz J Med Biol Res 2003[Feb]; 36 (2): 183-90Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death through the regulation of a number of Ca2+-dependent enzymes such as phospholipases, proteases, and nucleases. Mitochondria along with the endoplasmic reticulum play pivotal roles in regulating intracellular Ca2+ content. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. During cellular Ca2+ overload, mitochondria take up cytosolic Ca2+, which in turn induces opening of permeability transition pores and disrupts the mitochondrial membrane potential (deltapsim). The collapse of deltapsim along with the release of cytochrome c from mitochondria is followed by the activation of caspases, nuclear fragmentation and cell death. Members of the Bcl-2 family are a group of proteins that play important roles in apoptosis regulation. Members of this family appear to differentially regulate intracellular Ca2+ level. Translocation of Bax, an apoptotic signaling protein, from the cytosol to the mitochondrial membrane is another step in this apoptosis signaling pathway.|Animals[MESH]|Apoptosis/*physiology[MESH]|Calcium Signaling/*physiology[MESH]|Lymphokines/*physiology[MESH]|Mitochondria/*physiology[MESH]|Proto-Oncogene Proteins c-bcl-2/*physiology[MESH]|Proto-Oncogene Proteins/physiology[MESH]|bcl-2-Associated X Protein[MESH] |