Scientific article

Bcl-2 decreases the free Ca2+ concentration within the endoplasmic reticulum

Publication date2000

The antiapoptotic protein Bcl-2 localizes not only to mitochondria but also to the endoplasmic reticulum (ER). However, the function of Bcl-2 at the level of the ER is poorly understood. In this study, we have investigated the effects of Bcl-2 expression on Ca(2+) storage and release by the ER. The expression of Bcl-2 decreased the amount of Ca(2+) that could be released from intracellular stores, regardless of the mode of store depletion, the cell type, or the species from which Bcl-2 was derived. Bcl-2 also decreased cellular Ca(2+) store content in the presence of mitochondrial inhibitors, suggesting that its effects were not mediated through mitochondrial Ca(2+) uptake. Direct measurements with ER-targeted Ca(2+)-sensitive fluorescent "cameleon" proteins revealed that Bcl-2 decreased the free Ca(2+) concentration within the lumen of the ER, [Ca(2+)](ER). Analysis of the kinetics of Ca(2+) store depletion in response to the Ca(2+)-ATPase inhibitor thapsigargin revealed that Bcl-2 increased the permeability of the ER membrane. These results suggest that Bcl-2 decreases the free Ca(2+) concentration within the ER lumen by increasing the Ca(2+) permeability of the ER membrane. The increased ER Ca(2+) permeability conferred by Bcl-2 would be compatible with an ion channel function of Bcl-2 at the level of the ER membrane.

  • Animals
  • Apoptosis/physiology
  • Calcium/ metabolism
  • Calcium Signaling/physiology
  • Cell Line
  • Endoplasmic Reticulum/ metabolism
  • Fura-2/analogs & derivatives/metabolism
  • Genes, bcl-2
  • Humans
  • Intracellular Fluid/metabolism
  • Mice
  • Permeability
  • Proto-Oncogene Proteins c-bcl-2/ physiology
  • Recombinant Fusion Proteins/physiology
  • Transfection
  • Tumor Cells, Cultured
Citation (ISO format)
FOYOUZI-YOUSSEFI, Reyhaneh et al. Bcl-2 decreases the free Ca2+ concentration within the endoplasmic reticulum. In: Proceedings of the National Academy of Sciences of the United States of America, 2000, vol. 97, n° 11, p. 5723–5728.
Main files (1)
ISSN of the journal0027-8424

Technical informations

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First validation06/21/2010 10:24:05 AM
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