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• W2010649600 abstract "Calcium/phospholipid‐regulated protein kinase C (PKC) signalling is known to be involved in cellular functions relevant to brain health and disease, including ion channel modulation, receptor regulation, neurotransmitter release, synaptic plasticity, and survival. Brain aging is characterized by altered neuronal molecular cascades and interneuronal communication in response to various stimuli. In the last few years we have provided evidence that in rodents, despite no changes in PKC isoform levels (both calcium dependent and calcium independent), the activation/translocation process of the calcium‐dependent and ‐independent kinases and the content of the adaptor protein RACK1 (receptor for activated C kinase‐1) are deficient in physiological brain aging. Moreover, human studies have shown that PKC and its adaptor protein RACK1 are also interdependent in pathological brain aging (e.g., Alzheimer's disease); in fact, calcium‐dependent PKC translocation and RACK1 levels are both deficient in an area‐selective manner. These data point to the notion that, in addition to a well‐described lipid environment alteration, changes in protein‐protein interactions may impair the mechanisms of PKC activation in aging. It is interesting to note that interventions to counteract the age‐related functional loss also restore PKC activation and the adaptor protein machinery expression. A better insight into the factors controlling PKC activation may be important not only to elucidate the molecular basis of signal transmission, but also to identify new strategies to correct or even to prevent age‐dependent alterations in cell‐to‐cell communication." @default.
• W2010649600 created "2016-06-24" @default.
• W2010649600 creator A5026046616 @default.
• W2010649600 date "2005-12-01" @default.
• W2010649600 modified "2023-10-08" @default.
• W2010649600 title "Protein Kinase C Signal Transduction Regulation in Physiological and Pathological Aging" @default.
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• W2010649600 doi "https://doi.org/10.1196/annals.1356.011" @default.
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