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• W2049001528 endingPage "454" @default.
• W2049001528 startingPage "448" @default.
• W2049001528 abstract "The Prnd-encoded prion protein (PrP)-like protein, Doppel (Dpl), is a homologue of Prnp-encoded PrP, and is N-glycosylated protein with glycosylphosphatidylinositol anchor like PrP. Recently, ectopic expressions of Prnp/Prnd chimeric mRNAs have been identified as the cause of late-onset ataxia observed in several lines of Prnp-knockout mice such as ZrchII, Ngsk, Rcm0, and Rikn mice. However, it remains unclear whether the toxic effect of Dpl expression is a cell-autonomous mechanism but rather reflect a systemic process of heterogeneous cell population in the brain. In this study, the cell-autonomous role of Dpl was estimated by investigating PrP-deficient cells (HpL3-4)—the SV40 large T-antigen immortalized and Rikn Prnp−/− mice-derived neuronal cell line expressing Prnp/Prnd chimeric mRNAs. The reverse transcription polymerase chain reaction revealed that serum deprivation did not increase Prnp/Prnd chimeric mRNAs, which in fact was translated into a small amount of Dpl in HpL3-4 cells, whereas serum deprivation induced apoptotic cell death of HpL3-4 cells. Dpl overexpression enhanced apoptotic cell death, whereas the toxic effect of Dpl on apoptotic cell death was neutralized by PrP expression. These results indicate that Dpl elicited dose-dependently toxic effects on PrP-deficient cells without affecting on PrP-expressing cells, suggesting that the PrP–Dpl interaction can regulate cell death in a cell-autonomous manner." @default.
• W2049001528 created "2016-06-24" @default.
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• W2049001528 date "2005-07-01" @default.
• W2049001528 modified "2023-10-16" @default.
• W2049001528 title "Cell-autonomous PrP–Doppel interaction regulates apoptosis in PrP gene-deficient neuronal cells" @default.
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• W2049001528 doi "https://doi.org/10.1016/j.bbrc.2005.05.128" @default.
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