Molecular mechanisms mediating the neuroproyective effects of quinacrine and minocycline on cell death induced by the prion protein fragment 90-231 (hPrP90-231)

  • V. Villa
  • A. Corsaro
  • S. Thellung
  • A. Simi
  • M. Nizzari
  • M. Tonelli
  • V. Boido
  • A. Aceto
  • T. Florio | tullio.florio@unige.it

Abstract

The effects of quinacrine and minocycline on the toxicity induced by hPrP90-231 were studied. By mild thermal denaturation, hPrP90-231 can be converted in a toxic PrPSc-like structure affecting the survival of SH-SY5Y cells. Quinacrine and minocycline prevented hPrP90-231-induced toxicity interfering with different mechanisms: protective effects of quinacrine are mediated by the binding to the fragment that abolished hPrP90-231 structural changes and cell internalization, whereas, minocycline reverted MAP kinase neurotoxic signaling exerted by the prion fragment.

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Published
2011-01-30
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Abstract Book
Keywords:
prion protein, quinacrine, minocycline
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How to Cite
Villa, V., Corsaro, A., Thellung, S., Simi, A., Nizzari, M., Tonelli, M., Boido, V., Aceto, A., & Florio, T. (2011). Molecular mechanisms mediating the neuroproyective effects of quinacrine and minocycline on cell death induced by the prion protein fragment 90-231 (hPrP90-231). Journal of Biological Research - Bollettino Della Società Italiana Di Biologia Sperimentale, 84(1). https://doi.org/10.4081/jbr.2011.4689