Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Miller 2006 FEBS Lett"

From Bioblast
m (moved Miller 2006 FEBS Let to Miller 2006 FEBS Lett over redirect)
(No difference)

Revision as of 07:52, 2 July 2013

Publications in the MiPMap
Miller I, Gemeiner M, Gesslbauer B, Kungl A, Piskernik C, Haindl S, Nürnberger 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.

» PMID: 16442530

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 α 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

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