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首页> 外文期刊>Molecular and Cellular Biology >Lovastatin selectively inhibits ras activation of the 12-O-tetradecanoylphorbol-13-acetate response element in mammalian cells.
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Lovastatin selectively inhibits ras activation of the 12-O-tetradecanoylphorbol-13-acetate response element in mammalian cells.

机译:洛伐他汀在哺乳动物细胞中选择性抑制ras活化12-O-十四烷酰phorbol-13-乙酸盐响应元件。

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摘要

To evaluate ras-mediated signal transduction, an alkaline phosphatase gene (SEAP) was placed under the control of the ras-inducible phorbol ester response element (TRE) in murine fibroblasts (TRE-SEAP cells). The Kirsten ras gene was placed under the control of the glucocorticoid-inducible mouse mammary tumor virus promoter and introduced into the TRE-SEAP cells. Dexamethasone increased ras expression in the TRE-SEAP cells carrying the Kirsten ras gene and stimulated SEAP activity 25-fold. Lavostatin blocked dexamethasone induction of SEAP activity (50% inhibitory concentration, 0.5 microM) but did not affect phorbol ester-induced SEAP activity in the same cells. Lovastatin also did not block forskolin induction of SEAP activity in cells expressing SEAP under the control of the cyclic AMP response element.
机译:为了评估ras介导的信号转导,将碱性磷酸酶基因(SEAP)置于鼠成纤维细胞(TRE-SEAP细胞)中ras诱导佛波酯反应元件(TRE)的控制之下。将Kirsten ras基因置于糖皮质激素诱导的小鼠乳腺肿瘤病毒启动子的控制下,并将其引入TRE-SEAP细胞。地塞米松增加了携带Kirsten ras基因的TRE-SEAP细胞中的ras表达,并刺激了25倍的SEAP活性。 Lavostatin阻止地塞米松诱导SEAP活性(50%抑制浓度,0.5 microM),但不影响佛波酯诱导的SEAP活性。洛伐他汀在环状AMP应答元件的控制下,在表达SEAP的细胞中洛伐他汀也没有阻止福司可林诱导SEAP活性。

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