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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/9826

    Título
    WIP is a chaperone for Wiskott–Aldrich syndrome protein (WASP)
    Autor
    Fuente García, Miguel Ángel de laAutoridad UVA Orcid
    Sasahara, Yoji
    Calamito, Marco
    Antón, Inés María
    Elkhal, Abdallah
    Gallego, María Dolores
    Suresh, Koduro
    Siminovitch, Katherine
    Ochs, Hans D.
    Anderson, Kenneth C.
    Rosen, Fred S.
    Geha, Raif S.
    Ramesh, Narayanaswamy
    Año del Documento
    2007
    Editorial
    National Academy of Sciences
    Descripción
    Producción Científica
    Documento Fuente
    Proceedings of the National Academy of Sciences U S A. 2007 Jan 16;104(3):926-31
    Résumé
    Wiskott–Aldrich syndrome protein (WASP) is in a complex with WASP-interacting protein (WIP). WASP levels, but not mRNA levels, were severely diminished in T cells from WIP / mice and were increased by introduction of WIP in these cells. The WASP binding domain of WIP was shown to protect WASP from degradation by calpain in vitro. Treatment with the proteasome inhibitors MG132 and bortezomib increased WASP levels in T cells from WIP / mice and in T and B lymphocytes from two WAS patients with missense mutations (R86H and T45M) that disrupt WIP binding. The calpain inhibitor calpeptin increased WASP levels in activated T and B cells from the WASP patients, but not in primary T cells from the patients or from WIP / mice. Despite its ability to increase WASP levels proteasome inhibition did not correct the impaired IL-2 gene expression and low F-actin content in T cells from the R86H WAS patient. These results demonstrate that WIP stabilizes WASP and suggest that it may also be important for its function
    Materias (normalizadas)
    Wiskott Aldrich, Síndrome protéico
    ISSN
    0027-8424
    Revisión por pares
    SI
    DOI
    10.1073/pnas.0610275104
    Version del Editor
    https://www.pnas.org/content/104/3/926
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/9826
    Derechos
    openAccess
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    • DEP05 - Artículos de revista [198]
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