https://doi.org/10.4081/jbr.2011.4689

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

Vol. 84 No. 1 (2011)
Submitted: September 5, 2014
Accepted: September 5, 2014
Published: January 30, 2011
prion protein, quinacrine, minocycline
Abstract Views: 772
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Authors

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

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