Miller 2006 FEBS Lett
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