Long-term modulation of mitochondrial Ca2+ signals by protein kinase C isozymes

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Abstract

The modulation of Ca2+ signaling patterns during repetitive stimulations represents an important mechanism for integrating through time the inputs received by a cell. By either overexpressing the isoforms of protein kinase C (PKC) or inhibiting them with specific blockers, we investigated the role of this family of proteins in regulating the dynamic interplay of the intracellular Ca2+ pools. The effects of the different isoforms spanned from the reduction of ER Ca2+ release (PKCα) to the increase or reduction of mitochondrial Ca2+ uptake (PKCζ and PKCβ/PKCδ, respectively). This PKC-dependent regulatory mechanism underlies the process of mitochondrial Ca2+ desensitization, which in turn modulates cellular responses (e.g., insulin secretion). These results demonstrate that organelle Ca2+ homeostasis (and in particular mitochondrial processing of Ca2+ signals) is tuned through the wide molecular repertoire of intracellular Ca2+ transducers.

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Pinton, P., Leo, S., Wieckowski, M. R., Di Benedetto, G., & Rizzuto, R. (2004). Long-term modulation of mitochondrial Ca2+ signals by protein kinase C isozymes. Journal of Cell Biology, 165(2), 223–232. https://doi.org/10.1083/jcb.200311061

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