Cells are programmed to die when critical signaling and metabolic pathways are disrupted.
Inhibiting the type 2 ryanodine receptor (RyR2) in human and mouse pancreatic β-cells
markedly increased apoptosis. This mode of programmed cell death was not associated with
robust caspase-3 activation prompting a search for an alternative mechanism. Increased
calpain activity and calpain gene expression suggested a role for a calpain-dependent
death pathway. Using a combination of pharmacological and genetic approaches, we …