• español
  • English
  • français
  • Deutsch
  • português (Brasil)
  • italiano
    • español
    • English
    • français
    • Deutsch
    • português (Brasil)
    • italiano
    • español
    • English
    • français
    • Deutsch
    • português (Brasil)
    • italiano
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Listar

    Todo UVaDOCComunidadesPor fecha de publicaciónAutoresMateriasTítulos

    Mi cuenta

    Acceder

    Estadísticas

    Ver Estadísticas de uso

    Compartir

    Ver ítem 
    •   UVaDOC Principal
    • PRODUCCIÓN CIENTÍFICA
    • Departamentos
    • Dpto. Bioquímica y Biología Molecular y Fisiología
    • DEP06 - Artículos de revista
    • Ver ítem
    •   UVaDOC Principal
    • PRODUCCIÓN CIENTÍFICA
    • Departamentos
    • Dpto. Bioquímica y Biología Molecular y Fisiología
    • DEP06 - Artículos de revista
    • Ver ítem
    • español
    • English
    • français
    • Deutsch
    • português (Brasil)
    • italiano

    Exportar

    RISMendeleyRefworksZotero
    • edm
    • marc
    • xoai
    • qdc
    • ore
    • ese
    • dim
    • uketd_dc
    • oai_dc
    • etdms
    • rdf
    • mods
    • mets
    • didl
    • premis

    Citas

    Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/63896

    Título
    Altered succinylation of mitochondrial proteins, APP and tau in Alzheimer’s disease
    Autor
    Yang, Yun
    Tapias Molina, VictorAutoridad UVA Orcid
    Acosta, Diana
    Xu, Hui
    Chen, Huanlian
    Bhawal, Ruchika
    Anderson, Elizabeth T.
    Ivanova, Elena
    Lin, Hening
    Sagdullaev, Botir T.
    Chen, Jianer
    Klein, William L.
    Viola, Kirsten L.
    Gandy, Sam
    Haroutunian, Vahram
    Beal, M. Flint
    Eliezer, David
    Zhang, Sheng
    Gibson, Gary E.
    Año del Documento
    2022
    Descripción
    Producción Científica
    Documento Fuente
    Nature Communications, Enero 2022, vol. 13, n. 1. p. 159
    Resumen
    Abnormalities in brain glucose metabolism and accumulation of abnormal protein deposits called plaques and tangles are neuropathological hallmarks of Alzheimer’s disease (AD), but their relationship to disease pathogenesis and to each other remains unclear. Here we show that succinylation, a metabolism-associated post-translational protein modification (PTM), provides a potential link between abnormal metabolism and AD pathology. We quantified the lysine succinylomes and proteomes from brains of individuals with AD, and healthy controls. In AD, succinylation of multiple mitochondrial proteins declined, and succinylation of small number of cytosolic proteins increased. The largest increases occurred at critical sites of amyloid precursor protein (APP) and microtubule-associated tau. We show that in vitro, succinylation of APP disrupted its normal proteolytic processing thereby promoting Aβ accumulation and plaque formation and that succinylation of tau promoted its aggregation to tangles and impaired microtubule assembly. In transgenic mouse models of AD, elevated succinylation associated with soluble and insoluble APP derivatives and tau. These findings indicate that a metabolism-linked PTM may be associated with AD.
    Revisión por pares
    SI
    DOI
    10.1038/s41467-021-27572-2
    Idioma
    eng
    URI
    https://uvadoc.uva.es/handle/10324/63896
    Tipo de versión
    info:eu-repo/semantics/draft
    Derechos
    openAccess
    Aparece en las colecciones
    • DEP06 - Artículos de revista [352]
    Mostrar el registro completo del ítem
    Ficheros en el ítem
    Nombre:
    Yang et al 2022_Nat Commun.pdf
    Tamaño:
    4.202Mb
    Formato:
    Adobe PDF
    Thumbnail
    Visualizar/Abrir
    Atribución 4.0 InternacionalLa licencia del ítem se describe como Atribución 4.0 Internacional

    Universidad de Valladolid

    Powered by MIT's. DSpace software, Version 5.10