Trends in Microbiology
Volume 4, Issue 4, April 1996, Pages 129-131
CommentSleepless in Bologna: transmission of fatal familial insomia
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Cited by (23)
Prion diseases
2006, Emerging Foodborne PathogensHuman prion diseases: Epidemiology and integrated risk assessment
2003, Lancet NeurologyPrions and the Immune System: A Journey Through Gut, Spleen, and Nerves
2003, Advances in ImmunologyCitation Excerpt :Reintroduction of Prnp by transgenesis—even in a shortened, redacted form—restores infectibility and prion replication in Prnpo/o mice (Fischer et al., 1996; Shmerling et al., 1998; Supattapone et al., 1999; Flechsig et al., 2000). In addition, all familial cases of human TSEs are characterized by Prnp mutations (Aguzzi and Weissmann, 1996a; Prusiner et al., 1998). Informational nucleic acids of >50 nucleotides in length do not participate in prion infectivity (Kellings et al., 1993; Riesner et al., 1993), but shorter non-coding oligonucleotides have not been formally excluded—a fact that may have some relevance in view of the surprising discoveries related to RNA-mediated gene silencing.
The risk of transmission of variant Creutzfeldt-Jakob disease via contact lenses and ophthalmic devices
2002, Contact Lens and Anterior EyeSpongiform encephalopathies: Insights from transgenic models
2001, Advances in Virus ResearchPathogenesis of prion diseases: Possible implications of microglial cells
2001, Progress in Brain Research
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