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Induction of apoptosis by recombinant soluble human TRAIL in Jurkat cells / 生物医学与环境科学(英文)
Biomedical and Environmental Sciences ; (12): 470-477, 2007.
Artículo en Inglés | WPRIM | ID: wpr-249823
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the therapeutic potential of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a member of the TNF superfamily, and to analyze TRAIL-induced apoptosis in Jurkat cells.</p><p><b>METHODS</b>Expression of TRAIL receptors (DR4 and DR5) was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Cytotoxic effects were determined by colony formation assay and a cell counting kit. The effects of recombinant TRAIL on apoptosis of Jurkat cells were determined by DNA fragmentation (DNA ladder) and PI staining. Changes in mitochondrial membrane potential were detected with JC-1 fluorescence.</p><p><b>RESULTS</b>TRAIL inhibited the proliferation and induced internucleosomal DNA fragmentation (characteristic of apoptosis) and loss of mitochondrial membrane potential.</p><p><b>CONCLUSION</b>Recombinant soluble TRAIL can be used as a therapy for cancer.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Solubilidad / Proteínas Recombinantes / Secuencia de Bases / Apoptosis / Cartilla de ADN / Células Jurkat / Reacción en Cadena de la Polimerasa de Transcriptasa Inversa / Electroforesis en Gel de Agar / Ligando Inductor de Apoptosis Relacionado con TNF Límite: Humanos Idioma: Inglés Revista: Biomedical and Environmental Sciences Año: 2007 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Solubilidad / Proteínas Recombinantes / Secuencia de Bases / Apoptosis / Cartilla de ADN / Células Jurkat / Reacción en Cadena de la Polimerasa de Transcriptasa Inversa / Electroforesis en Gel de Agar / Ligando Inductor de Apoptosis Relacionado con TNF Límite: Humanos Idioma: Inglés Revista: Biomedical and Environmental Sciences Año: 2007 Tipo del documento: Artículo