Bcl-2 blocks deadly, persistent Ca2+ increases but allows signaling Ca2+ oscillations to proceed, according to Zhong et al. (page 127). As a result, this antiapoptotic protein can save T cells from death without interfering with other Ca2+-regulated cell functions.
Calcium has a hand in many physiological processes, including the proliferation of activated T cells. So the authors were a bit perplexed when they previously discovered that Bcl-2 inhibited IP3 receptors (IP3Rs), which release Ca2+ from the ER. But they now find that only persistent Ca2+ increases are affected by Bcl-2.
These persistent increases, or “transients,” result from high concentrations of antibodies, which activate T cell receptor (TCR) signaling and induce apoptosis. Although low antibody concentrations also activate TCRs, they lead to lasting Ca2+ oscillations that favor cell survival. These oscillations were not blocked...
