| Autor: |
Shi, Qi, Song, Qin-Qin, Sun, Peng, Zhang, Jin, Song, Juan, Chen, Li-Na, Xiao, Kang, Wang, Shao-Bin, Zhang, Ya-Zhou, Li, Gong-Qi, Sheng, Lin-Jun, Wang, Bao-Dong, Lu, Ming-Zhi, Han, Jun, Dong, Xiao-Ping |
| Zdroj: |
Molecular Neurobiology; Apr2014, Vol. 49 Issue 2, p840-851, 12p |
| Abstrakt: |
The 14-3-3 proteins are a family of highly homologous and ubiquitously expressed isoforms that are involved in a wide variety of physiological processes. 14-3-3 have showed actively molecular interaction with PrP and positive 14-3-3 is frequently observed in the cerebrospinal fluid (CSF) samples of the patients with sporadic Creutzfeldt-Jakob disease (CJD). However, the alterations of 14-3-3 in the brain tissues of patients with prion diseases remain little addressed. To address the possible change of brain 14-3-3 during prion infection, we firstly tested the levels of 14-3-3 in the brain tissues of scrapie agent 263 K infected hamsters. Obviously decreased 14-3-3 were observed in the samples of the infected animals, showing time-dependent reduction in the incubation period, while the amounts of S-nitrosylated 14-3-3 were increased in the brains collected at the late stage. A low level of 14-3-3 was also observed in the scrapie infectious cell line SMB-S15, accompanied with up-regulated Bax and down-regulated Bcl-2. Moreover, we found that treatment of PrP106-126 on the cultured cells decreased the cellular 14-3-3 and caused translocations of cellular Bax to the membrane fractions. Knockdown of cellular 14-3-3 sensitized the cultured cells to the challenge of PrP106-126. These data illustrate that significant down-regulation of brain 14-3-3 levels during prion infection may not only be a scenario of the terminal consequence of interacting with abnormal PrP but may also participate in the pathogenesis of neuronal damage. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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