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    • SCIENTIFIC PRODUCTION
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    • Dpto. Biología Celular, Genética, Histología y Farmacología
    • DEP05 - Artículos de revista
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    • DEP05 - Artículos de revista
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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/9843

    Título
    Defective nuclear translocation of nuclear factor of activated T cells and extracellular signal-regulated kinase underlies deficient IL-2 gene expression in Wiskott-Aldrich syndrome
    Autor
    Cianferoni, Antonella
    Massaad, Michel
    Feske, Stefan
    Fuente García, Miguel Ángel de laAutoridad UVA Orcid
    Gallego, María Dolores
    Ramesh, Narayanaswamy
    Geha, Raif S.
    Año del Documento
    2005
    Editorial
    Elsevier
    Descripción
    Producción Científica
    Documento Fuente
    Journal of Allergy and Clinical Immunology, 2005 ;116(6):1364-71.
    Abstract
    Background: Proliferation and IL-2 production in response to T-cell receptor ligation are impaired in patients with Wiskott- Aldrich syndrome (WAS). The transcription factors nuclear factor-kB (NF-kB), nuclear factor of activated T cells (NF-AT), and activating protein-1 (AP-1) play a critical role in IL-2 gene expression. Objective: To investigate the mechanisms of impaired IL-2 production after T-cell receptor ligation in T cells deficient in WAS protein (WASP). Methods: T cells from WASP2/2 mice were stimulated with anti-CD3 and anti-CD28. Nuclear NF-kB, NF-AT, and AP-1 DNA-binding activity was examined by electroshift mobility assay. NF-ATp dephosphorylation and nuclear localization were examined by Western blot and indirect immunofluorescence. Phosphorylation of the mitogen-activated protein kinases Erk and Jnk, and of their nuclear substrates Elk-1 and c-Jun, was examined by Western blot. Expression of mRNA for IL-2 and the NF-kB–dependent gene A20 and of the AP-1 components c-fos and c-Jun was examined by quantitative RT-PCR. Results: Nuclear translocation and activity of NF-kB were normal in T cells from WASP2/2 mice. In contrast, NF-ATp dephosphorylation and nuclear localization, nuclear AP-1 binding activity, and expression of c-fos, but not c-Jun, were all impaired. Phosphorylation of Jnk, c-Jun, and Erk were normal. However, nuclear translocation of phosphorylated Erk and phosphorylation of its nuclear substrate Elk1, which activates the c-fos promoter, were impaired. Conclusion: These results suggest that WASP is essential for NF-ATp activation, and for nuclear translocation of p-Erk, Elk1 phosphorylation, and c-fos gene expression in T cells. These defects underlie defective IL-2 expression and T-cell proliferation in WAS.
    Materias (normalizadas)
    Wiskott Aldrich, Síndrome
    Biología celular
    ISSN
    0091-6749
    Revisión por pares
    SI
    DOI
    10.1016/j.jaci.2005.09.006
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/9843
    Derechos
    openAccess
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    • DEP05 - Artículos de revista [126]
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