Reduced neuronal cell death after experimental brain injury in mice lacking a functional alternative pathway of complement activation-4

Copyright information:Taken from "Reduced neuronal cell death after experimental brain injury in mice lacking a functional alternative pathway of complement activation"BMC Neuroscience 2006;7():55-55.Published online 14 Jul 2006PMCID:PMC1540436.-PAGE, transferred to nitrocellulose membrane...

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Hauptverfasser: Leinhase, Iris, V Michael Holers, Thurman, Joshua M, Harhausen, Denise, Schmidt, Oliver I, Pietzcker, Malte, Mohy E Taha, Rittirsch, Daniel, Huber-Lang, Markus, Smith, Wade R, Ward, Peter A, Stahel, Philip F
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Sprache:eng
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Zusammenfassung:Copyright information:Taken from "Reduced neuronal cell death after experimental brain injury in mice lacking a functional alternative pathway of complement activation"BMC Neuroscience 2006;7():55-55.Published online 14 Jul 2006PMCID:PMC1540436.-PAGE, transferred to nitrocellulose membranes, and analyzed with specific monoclonal antibodies to Bcl-2, Fas, and β-actin as internal control and detection by chemiluminescence assay (ECLsystem, Amersham). () The visualized 26 kDa band corresponding to mouse Bcl-2 is enhanced in the knockout mice at 24 hours, compared to head-injured wild-type littermates. Furthermore, a downregulation in Fas receptor staining intensity is obvious in brain-injured knockout mice at all time-points assessed, compared to +/+ mice. The exemplary blot is representative of three independent experiments. () The individual band intensities of the blot shown in panel were quantified by TINA 2.09 software (Raytest, Straubenhardt, Germany) and the data are shown as relative levels to the according β-actin band intensity.
DOI:10.6084/m9.figshare.42319