Miller 2006 FEBS Lett: Difference between revisions
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{{Publication | {{Publication | ||
|title=Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, NΓΌrnberger S, Bahrami S, Redl H, Kozlov AV (2006) Proteome analysis of rat liver mitochondria reveals a possible compensatory response to endotoxic shock. FEBS Lett. 580: 1257-1262. | |title=Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, NΓΌrnberger S, Bahrami S, Redl H, Kozlov AV (2006) Proteome analysis of rat liver mitochondria reveals a possible compensatory response to endotoxic shock. FEBS Lett. 580: 1257-1262. | ||
|authors=Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, Nuernberger S,Β Bahrami S, Redl H, Kozlov AV Β | |authors=Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, Nuernberger S,Β Bahrami S, Redl H, Kozlov AV | ||
|year=2006 | |year=2006 | ||
|journal=FEBS Lett. | |journal=FEBS Lett. | ||
|mipnetlab=AT_Vienna_KozlovA | |mipnetlab=AT_Vienna_KozlovA | ||
|abstract=Organ failure induced by endotoxic shock has recently been associated with affected mitochondrial function. In this study, effects of in vivo lipopolysaccharide-challenge on protein patterns of rat liver mitochondria in treated animals versus controls were studied by two-dimensional electrophoresis (differential image gel electrophoresis). Significant upregulation was found for ATP-synthase Ξ± chain and superoxide dismutase [Mn]. Our data suggest that endotoxic shock mediated changes in the mitochondrial proteome contribute to a compensatory reaction (adaptation to endotoxic shock) rather than to a mechanism of cell damage. | |abstract=Organ failure induced by endotoxic shock has recently been associated with affected mitochondrial function. In this study, effects of in vivo lipopolysaccharide-challenge on protein patterns of rat liver mitochondria in treated animals versus controls were studied by two-dimensional electrophoresis (differential image gel electrophoresis). Significant upregulation was found for ATP-synthase Ξ± chain and superoxide dismutase [Mn]. Our data suggest that endotoxic shock mediated changes in the mitochondrial proteome contribute to a compensatory reaction (adaptation to endotoxic shock) rather than to a mechanism of cell damage. | ||
|keywords= Mitochondria, Proteomics, Lipopolysaccharide, Endotoxic shock, ATP-synthase, Superoxide dismutase | |keywords=Mitochondria, Proteomics, Lipopolysaccharide, Endotoxic shock, ATP-synthase, Superoxide dismutase | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16442530 PMID: 16442530] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/16442530 PMID: 16442530] | ||
}} | }} | ||
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|topics=Respiration; OXPHOS; ETS Capacity | |topics=Respiration; OXPHOS; ETS Capacity | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Revision as of 13:53, 20 October 2010
Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, NΓΌrnberger S, Bahrami S, Redl H, Kozlov AV (2006) Proteome analysis of rat liver mitochondria reveals a possible compensatory response to endotoxic shock. FEBS Lett. 580: 1257-1262. |
Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, Nuernberger S, Bahrami S, Redl H, Kozlov AV (2006) FEBS Lett.
Abstract: Organ failure induced by endotoxic shock has recently been associated with affected mitochondrial function. In this study, effects of in vivo lipopolysaccharide-challenge on protein patterns of rat liver mitochondria in treated animals versus controls were studied by two-dimensional electrophoresis (differential image gel electrophoresis). Significant upregulation was found for ATP-synthase Ξ± chain and superoxide dismutase [Mn]. Our data suggest that endotoxic shock mediated changes in the mitochondrial proteome contribute to a compensatory reaction (adaptation to endotoxic shock) rather than to a mechanism of cell damage. β’ Keywords: Mitochondria, Proteomics, Lipopolysaccharide, Endotoxic shock, ATP-synthase, Superoxide dismutase
β’ O2k-Network Lab: AT_Vienna_KozlovA
Labels:
Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Hepatocyte; Liver"Hepatocyte; Liver" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" 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