Abstract Book
Vol. 84 No. 1 (2011)
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)

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Received: 5 September 2014
Published: 30 January 2011
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prion protein, quinacrine, minocycline

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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Molecular mechanisms mediating the neuroproyective effects of quinacrine and minocycline on cell death induced by the prion protein fragment 90-231 (hPrP90-231). (2011). 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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