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Taxol induced Bcl-2 protein phosphorylation in human hepatocellular carcinoma QGY-7703 cell line.

机译:紫杉醇诱导人肝癌QGY-7703细胞株Bcl-2蛋白磷酸化。

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摘要

Bcl-2 family proteins play a critical role in the regulation of apoptosis. Treatment of a human hepatocellular carcinoma cell line, QGY-7703, with Taxol induced apoptosis and Bcl-2 protein phosphorylation. Microscopic observation indicated that apoptotic bodies (0-15%) of Taxol-treated QGY cells appeared after 12 h of treatment, and apoptotic QGY cells gradually increased to 40% after 24 h and 70% after 48 h. A DNA fragmentation assay showed that Taxol induced genomic DNA cleavage into 200 bp DNA fragments. Bcl-2 protein was phosphorylated in Taxol-treated QGY cells within 3 h of treatment, and continued gradually up to 24 h. By 48 h, the protein was unphosphorylated. Other Bcl-2 family proteins, including Bax (a heterodimerization partner of Bcl-2), Bcl-XL, Bak and Bad, were expressed, but at constant levels. The results show a close correlation between Bcl-2 phosphorylation and apoptosis in QGY cells. The inactivation of Bcl-2 protein phosphorylation could be one of the key mechanisms needed for the induction of apoptosis in Taxol-treated QGY cells. Copyright 2001 Academic Press.
机译:Bcl-2家族蛋白在细胞凋亡的调控中起着至关重要的作用。用紫杉酚诱导人肝癌细胞系QGY-7703的凋亡和Bcl-2蛋白磷酸化。显微镜观察表明,经紫杉醇处理的QGY细胞在处理12 h后出现凋亡小体(0-15%),凋亡的QGY细胞在24 h后逐渐增加至40%,在48 h后逐渐增加至70%。 DNA片段分析表明,紫杉酚诱导基因组DNA裂解为200 bp DNA片段。 Bcl-2蛋白在紫杉醇处理过的QGY细胞中在处理后3小时内被磷酸化,并持续持续到24小时。到48小时,该蛋白质未磷酸化。表达了其他Bcl-2家族蛋白,包括Bax(Bcl-2的异源二聚体伴侣),Bcl-XL,Bak和Bad,但含量恒定。结果表明,Bcl-2磷酸化与QGY细胞凋亡密切相关。 Bcl-2蛋白磷酸化的失活可能是诱导紫杉醇处理的QGY细胞凋亡所需的关键机制之一。版权所有2001,学术出版社。

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