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

Valentina Villa | Zendy; Alessandro Corsaro | Zendy; Stefano Thellung | Zendy; Alessandro Simi | Zendy; Mario Nizzari | Zendy; Michele Tonelli | Zendy; Vito Boido | Zendy; Antonio Aceto | Zendy; Tullio Florio | Zendy

Open Access

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

Author(s) -

Valentina Villa,

Alessandro Corsaro,

Stefano Thellung,

Alessandro Simi,

Mario Nizzari,

Michele Tonelli,

Vito Boido,

Antonio Aceto,

Tullio Florio

Publication year - 2011

Publication title -

journal of biological research - bollettino della società italiana di biologia sperimentale

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.218

H-Index - 6

eISSN - 2284-0230

pISSN - 1826-8838

DOI - 10.4081/jbr.2011.4689

Subject(s) - minocycline , internalization , toxicity , chemistry , cell , programmed cell death , protein kinase a , pharmacology , kinase , biochemistry , biology , apoptosis , antibiotics , organic chemistry

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 PrP^Sc-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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