ppat.1009991.s001.tif (2.42 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) Cellular functions and (B) metabolic pathways mainly affected by the absence of PrPC in 1C11 neuronal stem cells. Data are presented as the percentage of proteins involved in a specific cell function or metabolic pathway, whose expression is affected by the silencing of PrPC.
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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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