Creutzfeldt-Jakob Disease Research Today is a free monthly online journal that collates and summarizes the latest research about Creutzfeldt-Jakob Disease, including details on mad cow disease, symptoms, causes, variants. | ||||||||
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Different expression patterns of CK2 subunits in the brains of experimental animals and patients with transmissible spongiform encephalopathies.Chen JM, Gao C, Shi Q, Shan B, Lei YJ, Dong CF, An R, Wang GR, Zhang BY, Han J, Dong XP State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Ying-Xin Rd 100, 100052, Beijing, People’s Republic of China. To address the possible alteration of casein kinase 2 (CK2) in transmissible spongiform encephalopathies (TSEs), the levels and patterns of CK2 in the brain tissues of hamsters or C57BL mice inoculated intracerebrally with scrapie agents 263K or 139A were evaluated by Western blots, followed by quantitative analysis. Specific semi-quantitative RT-PCR for evaluating the mRNA transcripts of CK2 subunits was performed in parallel. Compared with normal animals, the levels of CK2alpha and CK2beta in the brains of infected hamsters and mice were significantly decreased, regardless of which scrapie agent was. However, the expression of CK2alpha' or CK2alpha'/CK2alpha'' in the animals infected with agents 263K or 139A was considerably increased. Furthermore, decreases of CK2alpha and CK2beta and increases of CK2alpha'/CK2alpha'' were observed in cerebella homogenates from one familial Creutzfeldt-Jakob disease (fCJD) case and one fatal familial insomnia (FFI) case. These results suggest that alterations of CK2 subunits in brains are illness-correlative phenomena in TSEs and indicate a potential linkage of CK2 changes with the pathogenesis of prion diseases. Published 10 June 2008 in Arch Virol, 153(6): 1013-1020.
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