BNIP3 in Cyanide-induced Brain Damage (Paperback)

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."

General

Imprint:	Lap Lambert Academic Publishing
Country of origin:	Germany
Release date:	July 2010
First published:	July 2010
Authors:	Lu Zhang
Dimensions:	229 x 152 x 11mm (L x W x T)
Format:	Paperback - Trade
Pages:	188
ISBN-13:	978-3-8383-5714-0
Categories:	Books > Medicine > Other branches of medicine > Pharmacology > General
LSN:	3-8383-5714-0
Barcode:	9783838357140

Is the information for this product incomplete, wrong or inappropriate? Let us know about it.

Does this product have an incorrect or missing image? Send us a new image.

Is this product missing categories? Add more categories.

Review This Product

No reviews yet - be the first to create one!