Miller 2006 FEBS Lett: Difference between revisions
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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 Let 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 Let
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_Kozlov AV
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: Liver
Coupling state: OXPHOS
HRR: Oxygraph-2k