ArticleMolecular neurobiology2014
Infection of prions and treatment of PrP106-126 alter the endogenous status of protein 14-3-3 and trigger the mitochondrial apoptosis possibly via activating Bax pathway.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 9 citations in OpenAlex.
- Different reactive profiles of calmodulin in the CSF samples of Chinese patients of four types of genetic prion diseases.Frontiers in molecular neuroscience · 2024Article
- Extensive Disturbances of Intracellular Components and Dysfunctions of Biological Pathways in the Brain Tissues During Prion Infection - China's Studies.China CDC weekly · 2022Review
- Aberrant Alterations of Mitochondrial Factors Drp1 and Opa1 in the Brains of Scrapie Experiment Rodents.Journal of molecular neuroscience : MN · 2017Article
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15 authors at 4 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
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(Sc) but may also participate in the pathogenesis of neuronal damage.
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