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Cell cycle-regulated transcription by the human immunodeficiency virus type 1 Tat transactivator.
Kashanchi, F; Agbottah, E T; Pise-Masison, C A; Mahieux, R; Duvall, J; Kumar, A; Brady, J N.
Afiliación
  • Kashanchi F; Virus Tumor Biology Section, Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
J Virol ; 74(2): 652-60, 2000 Jan.
Article en En | MEDLINE | ID: mdl-10623726
Cyclin-dependent kinases are required for the Tat-dependent transition from abortive to productive elongation. Further, the human immunodeficiency virus type 1 (HIV-1) Vpr protein prevents proliferation of infected cells by arresting them in the G(2) phase of the cell cycle. These findings suggest that the life cycle of the virus may be integrally related to the cell cycle. We now demonstrate by in vitro transcription analysis that Tat-dependent transcription takes place in a cell cycle-dependent manner. Remarkably, Tat activates gene expression in two distinct stages of the cell cycle. Tat-dependent long terminal repeat activation is observed in G(1). This activation is TAR dependent and requires a functional Sp1 binding site. A second phase of transactivation by Tat is observed in G(2) and is TAR independent. This later phase of transcription is enhanced by a natural cell cycle blocker of HIV-1, vpr, which arrests infected cells at the G(2)/M boundary. These studies link the HIV-1 Tat protein to cell cycle-specific biological functions.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación Viral de la Expresión Génica / Productos del Gen tat / Ciclo Celular / VIH-1 Límite: Humans Idioma: En Revista: J Virol Año: 2000 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación Viral de la Expresión Génica / Productos del Gen tat / Ciclo Celular / VIH-1 Límite: Humans Idioma: En Revista: J Virol Año: 2000 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos