Endoplasmic reticulum, Bcl-2 and Ca2+ handling in apoptosis

D. Ferrari, P. Pinton, G. Szabadkai, M. Chami, M. Campanella, T. Pozzan, Rosario Rizzuto

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)413-420
Number of pages8
JournalCell Calcium
Issue number5-6
Publication statusPublished - Nov 2002

ASJC Scopus subject areas

  • Cell Biology
  • Endocrinology


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