{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:06:43Z","timestamp":1791328003084,"version":"4.3.1"},"reference-count":69,"publisher":"National Academy of Sciences","issue":"26","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1997,12,23]]},"abstract":"<jats:p>\n                    There is considerable concern that bovine prions from cattle with bovine spongiform encephalopathy (BSE) may have been passed to humans (Hu), resulting in a new form of Creutzfeldt\u2013Jakob disease (CJD). We report here the transmission of bovine (Bo) prions to transgenic (Tg) mice expressing BoPrP; one Tg line exhibited incubation times of \u2248200 days. Like most cattle with BSE, vacuolation and astrocytic gliosis were confined in the brainstems of these Tg mice. Unexpectedly, mice expressing a chimeric Bo\/Mo PrP transgene were resistant to BSE prions whereas mice expressing Hu or Hu\/Mo PrP transgenes were susceptible to Hu prions. A comparison of differences in Mo, Bo, and Hu residues within the C terminus of PrP defines an epitope that modulates conversion of PrP\n                    <jats:sup>C<\/jats:sup>\n                    into PrP\n                    <jats:sup>Sc<\/jats:sup>\n                    and, as such, controls prion transmission across species. Development of susceptible Tg(BoPrP) mice provides a means of measuring bovine prions that may prove critical in minimizing future human exposure.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.26.14279","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:42:40Z","timestamp":1027680160000},"page":"14279-14284","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":128,"title":["Identification of a prion protein epitope modulating transmission of bovine spongiform encephalopathy prions to transgenic mice"],"prefix":"10.1073","volume":"94","author":[{"given":"Michael R.","family":"Scott","sequence":"first","affiliation":[{"name":"Departments of Neurology, Biochemistry and Biophysics, Medicine, Cellular and Molecular Pharmacology, and Pathology, University of California, San Francisco, CA 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