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The study investigates the cell death mechanisms triggered by cyanide exposure, focusing on the role of BNIP3 in dopaminergic cell lines. Cyanide activates the HIF-1 pathway, leading to increased BNIP3 expression, which initiates mitochondria-mediated apoptosis. In mice, sublethal cyanide doses elevate BNIP3 in the midbrain, correlating with dopaminergic neuron loss. BNIP3's localization in the endoplasmic reticulum and mitochondria enhances calcium release and uptake, while Bax co-localization with BNIP3 is crucial for mediating cell death through calcium signaling.
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BNIP3 in Cyanide-induced Brain Damage, Lu Zhang
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- Released
- 2010
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- (Paperback)
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