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Quantitative assessment of the degradation of aggregated TDP-43 mediated by the ubiquitin proteasome system and macroautophagy.
Cascella, Roberta; Fani, Giulia; Capitini, Claudia; Rusmini, Paola; Poletti, Angelo; Cecchi, Cristina; Chiti, Fabrizio.
  • Cascella R; Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.
  • Fani G; Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.
  • Capitini C; Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.
  • Rusmini P; Dipartimento di Scienze Farmacologiche e Biomolecolari, Centro di Eccellenza sulle Malattie Neurodegenerative, Università degli Studi di Milano, Milan, Italy.
  • Poletti A; Dipartimento di Scienze Farmacologiche e Biomolecolari, Centro di Eccellenza sulle Malattie Neurodegenerative, Università degli Studi di Milano, Milan, Italy.
  • Cecchi C; Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.
  • Chiti F; Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy; fabrizio.chiti@unifi.it.
FASEB J ; 31(12): 5609-5624, 2017 12.
Article en En | MEDLINE | ID: mdl-28842427
Amyotrophic lateral sclerosis and frontotemporal lobar degeneration with ubiquitin-positive inclusions are neurodegenerative disorders that share the cytosolic deposition of TDP-43 (TAR DNA-binding protein 43) in the CNS. TDP-43 is well known as being actively degraded by both the proteasome and macroautophagy. The well-documented decrease in the efficiency of these clearance systems in aging and neurodegeneration, as well as the genetic evidence that many of the familial forms of TDP-43 proteinopathies involve genes that are associated with them, suggest that a failure of these protein degradation systems is a major factor that contributes to the onset of TDP-43-associated disorders. Here, we inserted preformed human TDP-43 aggregates in the cytosol of murine NSC34 and N2a cells in diffuse form and observed their degradation under conditions in which exogenous TDP-43 is not expressed and endogenous nuclear TDP-43 is not recruited, thereby allowing a time zero to be established in TDP-43 degradation and to observe its disposal kinetically and analytically. TDP-43 degradation was observed in the absence and presence of selective inhibitors and small interfering RNAs against the proteasome and autophagy. We found that cytosolic diffuse aggregates of TDP-43 can be distinguished in 3 different classes on the basis of their vulnerability to degradation, which contributed to the definition-with previous reports-of a total of 6 distinct classes of misfolded TDP-43 species that range from soluble monomer to undegradable macroaggregates. We also found that the proteasome and macroautophagy-degradable pools of TDP-43 are fully distinguishable, rather than in equilibrium between them on the time scale required for degradation, and that a significant crosstalk exists between the 2 degradation processes.-Cascella, R., Fani, G., Capitini, C., Rusmini, P., Poletti, A., Cecchi, C., Chiti, F. Quantitative assessment of the degradation of aggregated TDP-43 mediated by the ubiquitin proteasome system and macroautophagy.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Autofagia / Ubiquitina / Complejo de la Endopetidasa Proteasomal / Proteínas de Unión al ADN Límite: Animals / Humans Idioma: En Año: 2017 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Autofagia / Ubiquitina / Complejo de la Endopetidasa Proteasomal / Proteínas de Unión al ADN Límite: Animals / Humans Idioma: En Año: 2017 Tipo del documento: Article