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- W2090840497 abstract "Insulin-like growth factor-1 (IGF-1) promotes the survival of cerebellar granule neurons by enhancing calcium influx through L-type calcium channels, whereas NMDA receptor-mediated calcium influx can lead to excitotoxic death. Here we demonstrate that L and NMDA receptor channel activities differentially regulate the transcription factor C/EBPβ to control neuronal survival. Specifically, we show that L channel-dependent calcium influx results in increased CaMKIV activity, which acts to decrease nuclear C/EBPβ levels. Conversely, NMDA receptor-mediated influx rapidly elevates nuclear C/EBPβ and induces excitotoxic death via activation of the calcium-dependent phosphatase, calcineurin. Moderate levels of AMPA receptor activity stimulate L channels to improve survival, whereas higher levels stimulate NMDA receptors and reduce neuronal survival, suggesting differential synaptic effects. Finally, N-type calcium channel activity reduces survival, potentially by increasing glutamate release. Together, these results show that the L-type calcium channel-dependent survival and NMDA receptor death pathways converge to regulate nuclear C/EBPβ levels, which appears to be pivotal in these mechanisms." @default.
- W2090840497 created "2016-06-24" @default.
- W2090840497 creator A5006784348 @default.
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- W2090840497 date "2003-08-01" @default.
- W2090840497 modified "2023-10-12" @default.
- W2090840497 title "Calcium Channel and NMDA Receptor Activities Differentially Regulate Nuclear C/EBPβ Levels to Control Neuronal Survival" @default.
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- W2090840497 doi "https://doi.org/10.1016/s0896-6273(03)00496-3" @default.
- W2090840497 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12925277" @default.
- W2090840497 hasPublicationYear "2003" @default.
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