ppat.1009991.s004.tif (2.44 MB)
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posted on 2021-10-05, 17:32 authored by Hélène Arnould, Vincent Baudouin, Anne Baudry, Luiz W. Ribeiro, Hector Ardila-Osorio, Mathéa Pietri, Cédric Caradeuc, Cynthia Soultawi, Declan Williams, Marjorie Alvarez, Carole Crozet, Fatima Djouadi, Mireille Laforge, Gildas Bertho, Odile Kellermann, Jean-Marie Launay, Gerold Schmitt-Ulms, Benoit Schneider(A) Representative western blot and quantification histogram of PDK4 protein expression level and (B) PDH activity in PC12 neuronal cells transiently silenced for PrPC expression (SiPrP) or not (SiScr) (n = 6). PC12 cells were treated with DCA (2 mM) for 6h. (C) Representative western blot and quantification histogram of PDK4 protein expression level and (D) PDH activity in primary cultures of hippocampal neurons isolated from adult FVB and PrP0/0-FVB mice and left to regenerate for 10 days (n = 6). Hippocampal neurons were treated with DCA (2 mM) for 6 h. GAPDH was used for normalization in western-blot experiments. Data are the mean ± SEM. *** denotes p < 0.001 and **** p < 0.0001.
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remain poorly elucidatedpotential therapeutic targetoxidative stress conditionsidentify therapeutic targetsfatty acids βbovine spongiform encephalopathiesmad cow diseasesc c study posits pdk4pyruvate dehydrogenase complexpathogenic prions prpglucose oxidative degradationdiv >< pprion protein controlcellular prion proteinprotein kinasejakob diseaseprion diseasessubsequent onsetplasma membranepdk4 extendspdk4 activitypdk4 ).neurodegeneration occurringmouse hippocampusmolecular pathwaysmetabolic roleinfected miceglobal approachesevent favorsenergetic metabolismdependent mannerbetter understandingbetter known
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