Induction of a mitogen-responsive gene after expression of the Ha-ras oncogene in NIH 3T3 fibroblasts
Induction of a mitogen-responsive gene after expression of the Ha-ras oncogene in NIH 3T3 fibroblasts
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在 NIH 3T3 成纤维细胞中表达 Ha-ras 癌基因后诱导丝裂原反应基因
DOI：
10.1128/mcb.9.11.5207-5214.1989
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发表时间：
1989
影响因子：
5.3
通讯作者：
R. Klemenz
中科院分区：
文献类型：
--
作者：
A. Werenskiold;S. Hoffmann;R. Klemenz
在Ha-ras(EJ)基因的条件性表达和静止的NIH3T3细胞有丝分裂激活后，已经分离到一个相应的cDNA克隆T1，其相应的mRNA在高水平的瞬时表达。糖皮质激素也刺激了T1的大量表达，但仅限于增殖细胞。至少有两条不同的信号通路参与了T1基因的调节：在没有p21ras的情况下，依赖于蛋白激酶C的信号参与了增殖的NIH3T3细胞对糖皮质激素的反应，而不依赖于蛋白激酶C的信号参与了对血清因子的反应。用蛋白激酶抑制剂2-氨基嘌呤处理细胞后，T1基因的表达被阻断。T1mRNA的积累在转录水平上受到调控。
A cDNA clone, T1, has been isolated whose corresponding mRNA was transiently expressed at highly elevated levels after conditional expression of the Ha-ras(EJ) gene and after mitogenic activation of quiescent NIH 3T3 cells. Glucocorticoid hormone stimulated substantial T1 expression as well but only in proliferating cells. At least two different signaling pathways participate in the regulation of the T1 gene: a protein kinase C-dependent signal is involved in the response of proliferating NIH 3T3 cells to glucocorticoid in the absence but not the presence of p21ras, whereas a protein kinase C-independent mechanism mediates the response to serum factors. Treatment of cells with the protein kinase inhibitor 2-aminopurine blocked induction of expression of the T1 gene. T1 mRNA accumulation is regulated at the transcriptional level.