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Difference between revisions of "Vrbacky 2003 Physiol Res"

From Bioblast
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{{Publication
{{Publication
|title=Vrbacky M, Krijt J, Drahota Z, Melkova Z (2003) Inhibitory effects of Bcl-2 on mitochondrial respiration. Physiol Res 52: 545-554.
|title=Vrbacky M, Krijt J, Drahota Z, Melkova Z (2003) Inhibitory effects of Bcl-2 on mitochondrial respiration. Physiol Res 52:545-54.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/14535829 PMID: 14535829]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/14535829 PMID: 14535829]
|authors=Vrbacky M, Krijt J, Drahota Z, Melkova Z
|authors=Vrbacky M, Krijt J, Drahota Z, Melkova Z
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}}
}}
{{Labeling
{{Labeling
|tissues=Endothelial; Epithelial; Mesothelial Cell
|tissues=Endothelial;epithelial;mesothelial cell
|model cell lines=HeLa, Other cell lines
|model cell lines=HeLa, Other cell lines
|preparations=Permeabilized cells
|preparations=Permeabilized cells

Revision as of 14:46, 17 February 2015

Publications in the MiPMap
Vrbacky M, Krijt J, Drahota Z, Melkova Z (2003) Inhibitory effects of Bcl-2 on mitochondrial respiration. Physiol Res 52:545-54.

Β» PMID: 14535829

Vrbacky M, Krijt J, Drahota Z, Melkova Z (2003) Physiol Res

Abstract: In contrast to the well-established anti-apoptotic effect of Bcl-2 protein, we have recently demonstrated that Bcl-2 overexpression by vaccinia virus causes apoptosis in BSC-40 cells, while it prevents apoptosis in HeLa G cells. Given the key role of mitochondria in the process of apoptosis, we focused on effects of Bcl-2 expression on mitochondrial energetics of these two cell lines. In this study we present data indicating that BSC-40 cells derive their ATP mainly from oxidative phosphorylation whereas HeLa G cells from glycolysis. More importantly, we show that in both cell lines, Bcl-2 inhibits mitochondrial respiration and causes a decrease of the ATP/ADP ratio. However, it appears that BSC-40 cells cannot sustain this decrease and die, while HeLa G cells survive, being adapted to the low ratio of ATP/ADP maintained by glycolysis. Based on this observation, we propose that the outcome of Bcl-2 expression is determined by the type of cellular ATP synthesis, namely that Bcl-2 causes apoptosis in cells relying on oxidative phosphorylation. β€’ Keywords: Bcl-2, Apoptosis, ATP, Mitochondrial respiration

β€’ O2k-Network Lab: CZ Prague Houstek J, CZ Hradec Kralove Cervinkova Z


Labels:

Stress:Cell death 

Tissue;cell: Endothelial;epithelial;mesothelial cell  Preparation: Permeabilized cells 

Regulation: ATP; ADP; AMP; PCr"ATP; ADP; AMP; PCr" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Substrate; Glucose; TCA Cycle"Substrate; Glucose; TCA Cycle" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k