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- W2028493513 abstract "Alterations in the functions of neuronal RNA-binding proteins (RBPs) can contribute to neurodegenerative diseases. However, neurons also express a set of widely distributed RBPs that may have developed specialized functions. Here, we show that the ubiquitous member of the otherwise neuronal Elavl/Hu family of RNA-binding proteins, Elavl1/HuR, has a neuroprotective role. Mice engineered to lack exclusively HuR in the hippocampal neurons of the central nervous system (CNS), maintain physiologic levels of neuronal Elavls and develop a partially diminished seizure response following strong glutamatergic excitation; however, they display an exacerbated neurodegenerative response subsequent to the initial excitotoxic event. This response was phenocopied in hippocampal cells devoid of ionotropic glutamate receptors in which the loss of HuR results in enhanced mitochondrial dysfunction, oxidative damage and programmed necrosis solely after glutamate challenge. The molecular dissection of HuR and nElavl mRNA targets revealed the existence of a HuR-restricted posttranscriptional regulon that failed in HuR-deficient neurons and is involved in cellular energetics and oxidation defense. Thus, HuR acts as a specialized controller of oxidative metabolism in neurons to confer protection from neurodegeneration." @default.
- W2028493513 created "2016-06-24" @default.
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- W2028493513 creator A5045271004 @default.
- W2028493513 creator A5085387169 @default.
- W2028493513 date "2014-10-10" @default.
- W2028493513 modified "2023-10-14" @default.
- W2028493513 title "Neuroprotection requires the functions of the RNA-binding protein HuR" @default.
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- W2028493513 doi "https://doi.org/10.1038/cdd.2014.158" @default.
- W2028493513 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4392069" @default.
- W2028493513 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25301069" @default.
- W2028493513 hasPublicationYear "2014" @default.
- W2028493513 type Work @default.