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Overexpression of neurogenin1 induces neurite outgrowth in F11 neuroblastoma cells
Experimental & Molecular Medicine ; : 469-475, 2002.
Artículo en Inglés | WPRIM | ID: wpr-13041
ABSTRACT
Neurogenin1 (Ngn1) is a basic helix-loop-helix (bHLH) transcription factor expressed in neuronal precursors in the developing nervous system. The function of Ngn1 in neurogenesis has been shown in various aspects. In this study, we investigated the neurogenic potential of Ngn1 using neuroblastoma cell line, F11, which could be induced to differentiate into neurons in the presence of cAMP. To investigate the expression of Ngn1, expression vectors for the full-length and the C- terminal deletion mutant of Ngn1 were constructed and their transactivation potential was verified using reporter gene containing the E-box sequence. Overexpression of the full-length Ngn1 induced neurite outgrowth in F11 cells in the absence of cAMP. A C-terminal deletion mutant, Ngn1(1-197), inhibited neurite outgrowth induced by cAMP in F11 cells. These results indicate that the Ngn1 plays an important role in differentiation of neuroblastoma cells and the C terminus of Ngn1 is essential for the efficient differentiation.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Factores de Transcripción / Regulación Neoplásica de la Expresión Génica / Diferenciación Celular / Activación Transcripcional / Western Blotting / Neuritas / Clonación Molecular / Secuencias Hélice-Asa-Hélice / ADN Complementario / AMP Cíclico Límite: Humanos Idioma: Inglés Revista: Experimental & Molecular Medicine Año: 2002 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Factores de Transcripción / Regulación Neoplásica de la Expresión Génica / Diferenciación Celular / Activación Transcripcional / Western Blotting / Neuritas / Clonación Molecular / Secuencias Hélice-Asa-Hélice / ADN Complementario / AMP Cíclico Límite: Humanos Idioma: Inglés Revista: Experimental & Molecular Medicine Año: 2002 Tipo del documento: Artículo