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Mitochondria are important regulators of cell death and cell survival. Mitochondrial Ca 2+  levels are critically involved in both of these processes. On the one hand, excessive mitochondrial Ca 2+  leads to Ca 2+ -induced mitochondrial outer membrane permeabilization and thus apoptosis. On the other hand, mitochondria need Ca 2+  in order to efficiently fuel the tricarboxylic acid cycle and maintain adequate mitochondrial bioenergetics. For obtaining this Ca 2+ , the mitochondria are largely dependent on close contact sites with the endoplasmic reticulum (ER), the so-called mitochondria-associated ER membranes. There, the inositol 1,4,5-trisphosphate receptors are responsible for the Ca 2+  release from the ER. It comes as no surprise that this Ca 2+  release from the ER and the subsequent Ca 2+  uptake at the mitochondria are finely regulated. Cancer cells often modulate ER-Ca 2+  transfer to the mitochondria in order to promote cell survival and to inhibit cell death. Important regulators of these Ca 2+  signals and the onset of cancer are the B-cell lymphoma 2 (Bcl-2) family of proteins. An increasing number of reports highlight the ability of these Bcl-2-protein family members to finely regulate Ca 2+  transfer from ER to mitochondria both in healthy cells and in cancer. In this review, we focus on recent insights into the dynamic regulation of ER–mitochondrial Ca 2+  fluxes by Bcl-2-family members and how this impacts cell survival, cell death and mitochondrial energy production.

Modulation of Ca2+ Signaling by Anti-apoptotic B-Cell Lymphoma 2 Proteins at the Endoplasmic Reticulum–Mitochondrial Interface