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

Cell Calcium. Nov-Dec 2002;32(5-6):413-20. doi: 10.1016/s0143416002002014.


In the complex signalling interplay that allows extracellular signals to be decoded into activation of apoptotic cell death, Ca(2+) plays a significant role. This is supported not only by evidence linking alterations in Ca(2+) 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 Ca(2+) 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 Ca(2+) store and (ii) this Ca(2+) 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Calcium / physiology*
  • Endoplasmic Reticulum / drug effects
  • Endoplasmic Reticulum / physiology*
  • Humans
  • Proto-Oncogene Proteins c-bcl-2 / physiology*


  • Proto-Oncogene Proteins c-bcl-2
  • Calcium

Grant support