Calcineurin-induced apoptosis and TMD

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Overexpression of calcineurin B in HEK 293 cells potentiated processing of caspase-3 and apoptosis triggered by tumor necrosis factor-α and cycloheximide treatment. In a cell-free system, overexpression of calcineurin B in HEK 293 cells markedly increased processing of caspase-3 by cytochrome c. Immunodepletion of calcineurin B from cytosolic extracts from Jurkat cells decreased processing of caspase-3 by cytochrome c. Knockdown of calcineurin B by RNA interference resulted in a reduced apoptosis in HEK293 cells, but not in caspase-3-deficient MCF-7 cells. These results suggest that calcineurin B may possess a novel function to participate in the regulation of apoptosis, in addition to its well-known ability to regulate calcineurin A. Furthermore, calcineurin B itself has no effect on apoptosis, but promotes apoptotic signal transduction system through the presentation of scaffold for the activation of caspase-3 by caspase-9. Therefore, calcineurin B may be useful for therapies to induce and promote apoptosis.