| Literature DB >> 17195841 |
Jürgen A Richt1, Poothappillai Kasinathan, Amir N Hamir, Joaquin Castilla, Thillai Sathiyaseelan, Francisco Vargas, Janaki Sathiyaseelan, Hua Wu, Hiroaki Matsushita, Julie Koster, Shinichiro Kato, Isao Ishida, Claudio Soto, James M Robl, Yoshimi Kuroiwa.
Abstract
Prion diseases are caused by propagation of misfolded forms of the normal cellular prion protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) in Creutzfeldt-Jakob disease (CJD) in humans. Disruption of PrP(C) expression in mice, a species that does not naturally contract prion diseases, results in no apparent developmental abnormalities. However, the impact of ablating PrP(C) function in natural host species of prion diseases is unknown. Here we report the generation and characterization of PrP(C)-deficient cattle produced by a sequential gene-targeting system. At over 20 months of age, the cattle are clinically, physiologically, histopathologically, immunologically and reproductively normal. Brain tissue homogenates are resistant to prion propagation in vitro as assessed by protein misfolding cyclic amplification. PrP(C)-deficient cattle may be a useful model for prion research and could provide industrial bovine products free of prion proteins.Entities:
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Year: 2006 PMID: 17195841 PMCID: PMC2813193 DOI: 10.1038/nbt1271
Source DB: PubMed Journal: Nat Biotechnol ISSN: 1087-0156 Impact factor: 54.908