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10.1038/srep17146

http://scihub22266oqcxt.onion/10.1038/srep17146
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C4683536!4683536!26679898
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suck abstract from ncbi


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pmid26679898      Sci+Rep 2015 ; 5 (ä): ä
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  • Prion protein localizes at the ciliary base during neural and cardiovascular development, and its depletion affects ?-tubulin post-translational modifications #MMPMID26679898
  • Halliez S; Martin-Lannerée S; Passet B; Hernandez-Rapp J; Castille J; Urien C; Chat S; Laude H; Vilotte JL; Mouillet-Richard S; Béringue V
  • Sci Rep 2015[]; 5 (ä): ä PMID26679898show ga
  • Although conversion of the cellular form of the prion protein (PrPC) into a misfolded isoform is the underlying cause of prion diseases, understanding PrPC physiological functions has remained challenging. PrPC depletion or overexpression alters the proliferation and differentiation properties of various types of stem and progenitor cells in vitro by unknown mechanisms. Such involvement remains uncertain in vivo in the absence of any drastic phenotype of mice lacking PrPC. Here, we report PrPC enrichment at the base of the primary cilium in stem and progenitor cells from the central nervous system and cardiovascular system of developing mouse embryos. PrPC depletion in a neuroepithelial cell line dramatically altered key cilium-dependent processes, such as Sonic hedgehog signalling and ?-tubulin post-translational modifications. These processes were also affected over a limited time window in PrPC?ablated embryos. Thus, our study reveals PrPC as a potential actor in the developmental regulation of microtubule dynamics and ciliary functions.
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