BNIP3 in Cyanide-induced Brain Damage: The Involvement of BNIP3 and Calcium in Cyanide-induced Neurotoxicity

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Įprasta kaina: 97,88 
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Kupono kodas: ENG15
Akcija baigiasi: 2025-03-03
-15% su kodu: ENG15
83,20 
Įprasta kaina: 97,88 
-15% su kodu: ENG15
Kupono kodas: ENG15
Akcija baigiasi: 2025-03-03
-15% su kodu: ENG15
2025-02-28 97.8800 InStock
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Knygos aprašymas

In this study, an immortalized dopaminergic cell line was used to characterize the cell death signaling cascade activated by cyanide. Cyanide activated the HIF-1¿-mediated pathway of BNIP3 induction through a redox-sensitive process. Increased BNIP3 expression then served as an initiator of mitochondria-mediated death. In mice, repeated exposure to a sublethal dose of cyanide resulted in an increase of BNIP3 expression in midbrain, which was accompanied by a loss of dopaminergic neurons. In cortex, cyanide induced upregulation of BNIP3, which may be involved in cortical cell apoptosis. It is also shown that BNIP3 was localized in both ER and mitochondria to facilitate the release of Ca2+ from ER and subsequently increase uptake of Ca2+ into mitochondria. Excessive accumulation of mitochondrial Ca2+ facilitated the loss of ¿¿m, ultimately resulting in the execution of cell death. Current results also confirm that Bax was activated and co-localized with BNIP3 in ER and mitochondria. Acting as a downstream effector for BNIP3, Bax is required for Ca2+ crosstalk between ER and mitochondria, thereby contributing to mitochondria-mediated cell apoptosis.

Informacija

Autorius: Lu Zhang
Leidėjas: LAP LAMBERT Academic Publishing
Išleidimo metai: 2010
Knygos puslapių skaičius: 188
ISBN-10: 3838357140
ISBN-13: 9783838357140
Formatas: 220 x 150 x 12 mm. Knyga minkštu viršeliu
Kalba: Anglų

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