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Dysregulated proteostasis network in neuronal diseases.
Tseng, Ching-San; Chao, Yu-Wen; Liu, Yi-Hsiang; Huang, Yi-Shuian; Chao, Hsu-Wen.
Afiliación
  • Tseng CS; Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
  • Chao YW; Department of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
  • Liu YH; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
  • Huang YS; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
  • Chao HW; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Front Cell Dev Biol ; 11: 1075215, 2023.
Article en En | MEDLINE | ID: mdl-36910151
Long-term maintenance of synaptic connections is important for brain function, which depends on varying proteostatic regulations to govern the functional integrity of neuronal proteomes. Proteostasis supports an interconnection of pathways that regulates the fate of proteins from synthesis to degradation. Defects in proteostatic signaling are associated with age-related functional decline and neurodegenerative diseases. Recent studies have advanced our knowledge of how cells have evolved distinct mechanisms to safely control protein homeostasis during synthesis, folding and degradation, and in different subcellular organelles and compartments. Neurodegeneration occurs when these protein quality controls are compromised by accumulated pathogenic proteins or aging to an irreversible state. Consequently, several therapeutic strategies, such as targeting the unfolded protein response and autophagy pathways, have been developed to reduce the burden of misfolded proteins and proved useful in animal models. Here, we present a brief overview of the molecular mechanisms involved in maintaining proteostatic networks, along with some examples linking dysregulated proteostasis to neuronal diseases.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Front Cell Dev Biol Año: 2023 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Front Cell Dev Biol Año: 2023 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Suiza