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Involvement of 14-3-3 in tubulin instability and impaired axon development is mediated by Tau
Joo, Yuyoung,Schumacher, Benjamin,Landrieu, Isabelle,Bartel, Maria,Smet-Nocca, Caroline,Jang, Ahram,Choi, Hee Soon,Jeon, Noo Li,Chang, Keun-A,Kim, Hye-Sun,Ottmann, Christian,Suh, Yoo-Hun The Federation of American Societies for Experimen 2015 The FASEB Journal Vol.29 No.10
<P>14-3-3 proteins act as adapters that exert their function by interacting with their various protein partners. 14-3-3 proteins have been implicated in a variety of human diseases including neurodegenerative diseases. 14-3-3 proteins have recently been reported to be abundant in the neurofibrillary tangles (NFTs) observed inside the neurons of brains affected by Alzheimer’s disease (AD). These NFTs are mainly constituted of phosphorylated Tau protein, a microtubule-associated protein known to bind 14-3-3. Despite this indication of 14-3-3 protein involvement in the AD pathogenesis, the role of 14-3-3 in the Tauopathy remains to be clarified. In the present study, we shed light on the role of 14-3-3 proteins in the molecular pathways leading to Tauopathies. Overexpression of the 14-3-3σ isoform resulted in a disruption of the tubulin cytoskeleton and prevented neuritic outgrowth in neurons. NMR studies validated the phosphorylated residues pSer214 and pSer324 in Tau as the 2 primary sites for 14-3-3 binding, with the crystal structure of 14-3-3σ in complex with Tau-pSer214 and Tau-pSer324 revealing the molecular details of the interaction. These data suggest a rationale for a possible pharmacologic intervention of the Tau/14-3-3 interaction.—Joo, Y., Schumacher, B., Landrieu, I., Bartel, M., Smet-Nocca, C., Jang, A., Choi, H. S., Jeon, N. L., Chang, K.-A., Kim, H.-S., Ottmann, C., Suh, Y.-H. Involvement of 14-3-3 in tubulin instability and impaired axon development is mediated by Tau.</P>
( Roberto Scatena ),( Irene Messana ),( Giuseppe Ettore Martorana ),( Maria Luisa Gozzo ),( Silvio Lippa ),( Alessandro Maccaglia ),( Patrizia Bottoni ),( Federica Vincenzoni ),( Giuseppina Nocca ),( 생화학분자생물학회 2004 BMB Reports Vol.37 No.4
Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% 0₂, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondria) respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondria) activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ⅱ) induction of metabolic compensatory adaptations, with significant shift to glycolysis; ⅲ) induction of different antioxidant enzyme activities; ⅳ) significant cell growth inhibition and ⅴ) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.
Scatena, Roberto,Messana, Irene,Martorana, Giuseppe Ettore,Gozzo, Maria Luisa,Lippa, Silvio,Maccaglia, Alessandro,Bottoni, Patrizia,Vincenzoni, Federica,Nocca, Giuseppina,Castagnola, Massimo,Giardina, Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% $O_2$, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondrial respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondrial activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ii) induction of metabolic compensatory adaptations, with significant shift to glycolysis; iii) induction of different antioxidant enzyme activities; iv) significant cell growth inhibition and v) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.