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Defective activation and survival of T cells lacking the Ets-1 transcription factor.
Muthusamy, N; Barton, K; Leiden, J M.
Afiliación
  • Muthusamy N; Department of Medicine, University of Chicago, Illinois 60637, USA.
Nature ; 377(6550): 639-42, 1995 Oct 19.
Article en En | MEDLINE | ID: mdl-7566177
The Ets-1 proto-oncogene is a member of the Ets family of eukaryotic transcription factors. Members of this family play important roles in regulating gene expression in response to multiple developmental and mitogenic signals. Ets-1 is preferentially expressed at high levels in B and T cells of adult mice and is regulated during both thymocyte development and T-cell activation. To study the role of Ets-1 in T-cell development and function we have used the RAG-2-/- complementation system and murine embryonic stem (ES) cells containing homozygous deletions in the Ets-1 gene (Ets-1-/-). Ets-1-/(-)-RAG-2-/- chimaeric mice displayed markedly decreased numbers of mature thymocytes and peripheral T cells. Ets-1-/- T cells expressed normal levels of CD3 and T-cell antigen receptor (TCR)-alpha/beta. However, they displayed a severe proliferative defect in response to multiple activational signals and demonstrated increased rates of spontaneous apoptosis in vitro. These findings demonstrate that Ets-1 is required for the normal survival and activation of murine T cells.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Activación de Linfocitos / Linfocitos T / Supervivencia Celular / Proteínas Proto-Oncogénicas / Proteínas de Unión al ADN Límite: Animals Idioma: En Revista: Nature Año: 1995 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Activación de Linfocitos / Linfocitos T / Supervivencia Celular / Proteínas Proto-Oncogénicas / Proteínas de Unión al ADN Límite: Animals Idioma: En Revista: Nature Año: 1995 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido