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- W2420736215 abstract "Abstract In neurons, enhanced protein kinase A (PKA) signaling elevates synaptic plasticity, promotes neuronal development, and increases dopamine synthesis. By contrast, a decline in PKA signaling contributes to the etiology of several brain degenerative diseases, including Alzheimer’s disease and Parkinson’s disease, suggesting that PKA predominantly plays a neuroprotective role. A-kinase anchoring proteins (AKAPs) are large multidomain scaffold proteins that target PKA and other signaling molecules to distinct subcellular sites to strategically localize PKA signaling at dendrites, dendritic spines, cytosol, and axons. PKA can be recruited to the outer mitochondrial membrane by associating with three different AKAPs to regulate mitochondrial dynamics, structure, mitochondrial respiration, trafficking, dendrite morphology, and neuronal survival. In this review, we survey the myriad of essential neuronal functions modulated by PKA but place a special emphasis on mitochondrially localized PKA. Finally, we offer an updated overview of how loss of PKA signaling contributes to the etiology of several brain degenerative diseases." @default.
- W2420736215 created "2016-06-24" @default.
- W2420736215 creator A5076515369 @default.
- W2420736215 creator A5077998739 @default.
- W2420736215 date "2015-01-01" @default.
- W2420736215 modified "2023-09-30" @default.
- W2420736215 title "Role of protein kinase A in regulating mitochondrial function and neuronal development: implications to neurodegenerative diseases" @default.
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- W2420736215 doi "https://doi.org/10.1515/revneuro-2014-0085" @default.
- W2420736215 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4437841" @default.
- W2420736215 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25741943" @default.
- W2420736215 hasPublicationYear "2015" @default.
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