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- W2065671606 abstract "Nerve growth factor (NGF) readdition to NGF-deprived neurons can halt Jun N-terminal kinase (JNK) activation, cytochrome c release, and cell death through mechanisms that may involve phosphatidylinositol (PI) 3-kinase, Akt, and nuclear factor kappa B (NF-κB). We found that expression of the NF-κB protein c-Rel in NGF-deprived neurons blocks cytochrome c release but does not inhibit c-Jun phosphorylation. Conversely, inhibition of NF-κB in NGF-maintained neurons promotes cytochrome c release and cell death. In contrast to c-Rel, activated PI 3-kinase and Akt inhibit c-Jun phosphorylation but have only a small effect on cytochrome c release. Finally, although c-Rel can protect neurons from death caused by inhibitors of PI 3-kinase or Akt, NF-κB function is not critical for Akt-promoted survival. These results suggest that the PI 3-kinase/Akt and NF-κB survival pathways target distinct cell death events in neurons." @default.
- W2065671606 created "2016-06-24" @default.
- W2065671606 creator A5061838572 @default.
- W2065671606 creator A5071919602 @default.
- W2065671606 date "2001-09-01" @default.
- W2065671606 modified "2023-10-12" @default.
- W2065671606 title "Analysis of the NF-κB and PI 3-Kinase/Akt Survival Pathways in Nerve Growth Factor-Dependent Neurons" @default.
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- W2065671606 doi "https://doi.org/10.1006/mcne.2001.1021" @default.
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