Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 류종석 | - |
dc.date.accessioned | 2018-10-18T08:12:40Z | - |
dc.date.available | 2018-10-18T08:12:40Z | - |
dc.date.issued | 2009-11 | - |
dc.identifier.citation | ANTIVIRAL RESEARCH, v. 84, No. 2, Page. 185-193 | en_US |
dc.identifier.issn | 0166-3542 | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S0166354209004550 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/76569 | - |
dc.description.abstract | Prion diseases are incurable, transmissible neurodegenerative disorders in humans and animals. Because the disease-associated isoform of prion protein, PrPSc, is conformationally converted from cellular prion protein, PrPC, knockdown of PrPC expression by RNA interference (RNAi) implicates therapy for prion diseases. In this study, introduction of small interfering (si) and small hairpin (sh) RNAs targeting the prion protein gene (prnp) transcripts triggered specific gene silencing and reduced the PrPC level in both prion-free and -infected neuroblastoma cell lines. Furthermore, this approach suppressed PrPSc formation and ultimately eliminated PrPSc from prion-infected cell lines. However, prolonged culture of cured cells resulted in reappearance of PrPSc in the cell population, presumably by de novo PrPSc formation from residual PrPC uncontrolled by RNAi and PrPSc remained under the detection limit. Protein misfolding cyclic amplification assays further confirmed that lysate of cured cells was sufficient to support PrPSc propagation. Our data not only suggest a potential treatment option but also implicate a caveat for using an RNAi approach for prion diseases. These findings provide critical information required to advance RNAi-based prevention and therapy for prion diseases of humans and animals. (C) 2009 Elsevier B.V. All rights reserved. | en_US |
dc.description.sponsorship | The authors thank Dr. Glenn Telling (University of Kentucky) for his generous gift of Tg4112 mouse brains and technical consultation on PMCA, and Ms. Paula Thomason for editing this manuscript. This work was supported in part by funds from the Sanders Brown Center on Aging and College of Medicine, University of Kentucky. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | ELSEVIER SCIENCE BV | en_US |
dc.subject | Prion | en_US |
dc.subject | PrP(C) | en_US |
dc.subject | PrP(Sc) | en_US |
dc.subject | RNAi | en_US |
dc.subject | siRNA | en_US |
dc.subject | shRNA | en_US |
dc.title | Utility of RNAi-mediated prnp gene silencing in neuroblastoma cells permanently infected by prions: Potentials and limitations | en_US |
dc.type | Article | en_US |
dc.relation.volume | 84 | - |
dc.identifier.doi | 10.1016/j.antiviral.2009.09.002 | - |
dc.relation.page | 185-193 | - |
dc.relation.journal | ANTIVIRAL RESEARCH | - |
dc.contributor.googleauthor | Kim, Younghwan | - |
dc.contributor.googleauthor | Han, Boram | - |
dc.contributor.googleauthor | Titlow, William | - |
dc.contributor.googleauthor | Mays, Charles E. | - |
dc.contributor.googleauthor | Kwon, Moosik | - |
dc.contributor.googleauthor | Ryou, Chongsuk | - |
dc.relation.code | 2009200804 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF PHARMACY[E] | - |
dc.sector.department | DEPARTMENT OF PHARMACY | - |
dc.identifier.pid | cryou2 | - |
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