Ferrari, D; Pinton, P; Szabadkai, G; Chami, M; Campanella, M; Pozzan, T; Rizzuto, R; (2002) Endoplasmic reticulum, Bcl-2 and Ca2+ handling in apoptosis. CELL CALCIUM , 32 (5-6) 413 - 420. 10.1016/S0143-4160(02)00201-4.
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In the complex signalling interplay that allows extracellular signals to be decoded into activation of apoptotic cell death, Ca2+ plays a significant role. This is supported not only by evidence linking alterations in Ca2+ homeostasis to the triggering of apoptotic (and in some cases necrotic) cell death, but also by recent data indicating that a key anti-apoptotic protein, Bcl-2, has a direct effect on ER Ca2+ handling. We-will briefly summarise the first aspect, and describe in more detail these new data, demonstrating that (i) Bcl-2 reduces the state of filling of the ER Ca2+ store and (ii) this Ca2+ signalling alteration renders the cells less sensitive to apoptotic stimuli. Overall, these results suggest that calcium homeostasis may represent a pharmacological target in the fundamental pathological process of apoptosis. (C) 2002 Elsevier Science Ltd. All rights reserved.
|Title:||Endoplasmic reticulum, Bcl-2 and Ca2+ handling in apoptosis|
|Keywords:||PROTEIN-KINASE-C, INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR, METHYL-D-ASPARTATE, CELL-DEATH, CALCIUM IONOPHORE, CYTOCHROME-C, CANCER CELLS, MITOCHONDRIA, ACTIVATION, RELEASE|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Life Sciences > Biosciences (Division of) > Cell and Developmental Biology|
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