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- W1963674319 abstract "Changes in O2 tension can significantly impact cell survival, yet the mechanisms underlying these effects are not well understood. Here, we report that maintaining sympathetic neurons under low O2 inhibits apoptosis caused by NGF deprivation. Low O2 exposure blocked cytochrome c release after NGF withdrawal, in part by suppressing the up-regulation of BIMEL. Forced BIMEL expression removed the block to cytochrome c release but did not prevent protection by low O2. Exposing neurons to low O2 also activated hypoxia-inducible factor (HIF) and expression of a stabilized form of HIF-1α (HIF-1αPP→AG) inhibited cell death in normoxic, NGF-deprived cells. Targeted deletion of HIF-1α partially suppressed the protective effect of low O2, whereas deletion of HIF-1α combined with forced BIMEL expression completely reversed the ability of low O2 to inhibit cell death. These data suggest a new model for how O2 tension can influence apoptotic events that underlie trophic factor deprivation–induced cell death." @default.
- W1963674319 created "2016-06-24" @default.
- W1963674319 creator A5000205436 @default.
- W1963674319 creator A5071919602 @default.
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- W1963674319 date "2005-03-14" @default.
- W1963674319 modified "2023-10-13" @default.
- W1963674319 title "Inhibition of NGF deprivation–induced death by low oxygen involves suppression of BIMEL and activation of HIF-1" @default.
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- W1963674319 doi "https://doi.org/10.1083/jcb.200407079" @default.
- W1963674319 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2171791" @default.
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