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


Submitted: September 5, 2014
Accepted: September 5, 2014
Published: January 30, 2011
Abstract Views: 720
PDF: 493
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Authors

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.

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

Downloads

Download data is not yet available.

Citations