在NIH 3T3成纤维细胞中表达Ha-ras癌基因后诱导有丝分裂原反应基因。
Induction of a mitogen-responsive gene after expression of the Ha-ras oncogene in NIH 3T3 fibroblasts.
作者信息
Werenskiold A K, Hoffmann S, Klemenz R
机构信息
Ludwig Institute for Cancer Research, Inselspita, Bern, Switzerland.
出版信息
Mol Cell Biol. 1989 Nov;9(11):5207-14. doi: 10.1128/mcb.9.11.5207-5214.1989.
Abstract
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.
摘要
已分离出一个cDNA克隆T1，其相应的mRNA在Ha-ras（EJ）基因的条件性表达后以及静止的NIH 3T3细胞有丝分裂激活后以高度升高的水平瞬时表达。糖皮质激素也能刺激T1的大量表达，但仅在增殖细胞中。至少有两条不同的信号通路参与T1基因的调控：在不存在p21ras但存在糖皮质激素的情况下，蛋白激酶C依赖性信号参与增殖的NIH 3T3细胞对糖皮质激素的反应，而蛋白激酶C非依赖性机制介导对血清因子的反应。用蛋白激酶抑制剂2-氨基嘌呤处理细胞可阻断T1基因表达的诱导。T1 mRNA的积累在转录水平受到调控。
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