Your browser doesn't support javascript.
loading
Effects of overexpression of PEMT2 on expression and translocation of different PKC isoforms in rat hepatoma cells / 中华肝脏病杂志
Chinese Journal of Hepatology ; (12): 678-681, 2005.
Artículo en Chino | WPRIM | ID: wpr-276389
ABSTRACT
<p><b>OBJECTIVE</b>To explore the mechanism of cell proliferation inhibition by transfecting phosphatidylethanolamine N-methyltransferase 2 gene (PEMT2).</p><p><b>METHODS</b>The expression and translocation of different isoforms of protein kinase C (PKC) in cells were observed with immunocytochemistry and Western blot techniques. The content of diacylglycerol (DAG) was analyzed with high performance thin layer chromatography (HPTLC) technique.</p><p><b>RESULTS</b>Transfection of PEMT2 can inhibit the expression of cPKC alpha, but obviously promotes the expression and translocation from cytosol to plasma membrane of cPKC beta2. At the same time, the content of DAG was decreased in the transfected cells. Expression and translocation of other PKC isoforms were not changed by PEMT2 transfection.</p><p><b>CONCLUSION</b>Effects of overexpression of PEMT2 on the expression and translocation of different PKC isoforms might be related to the mechanism of cell proliferation inhibition and apoptosis induced by transfecting PEMT2.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Proteína Quinasa C / Transfección / Isoformas de Proteínas / Fosfatidiletanolamina N-Metiltransferasa / Genética / Neoplasias Hepáticas Experimentales Límite: Animales Idioma: Chino Revista: Chinese Journal of Hepatology Año: 2005 Tipo del documento: Artículo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Proteína Quinasa C / Transfección / Isoformas de Proteínas / Fosfatidiletanolamina N-Metiltransferasa / Genética / Neoplasias Hepáticas Experimentales Límite: Animales Idioma: Chino Revista: Chinese Journal of Hepatology Año: 2005 Tipo del documento: Artículo