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人核糖体蛋白L7的组成型表达使细胞周期停滞于G1期,并诱导Jurkat T淋巴瘤细胞凋亡。

Constitutive expression of human ribosomal protein L7 arrests the cell cycle in G1 and induces apoptosis in Jurkat T-lymphoma cells.

作者信息

Neumann F, Krawinkel U

机构信息

Faculty of Biology, University of Konstanz, Germany.

出版信息

Exp Cell Res. 1997 Feb 1;230(2):252-61. doi: 10.1006/excr.1996.3417.

Abstract

Protein L7 is involved in translational control in eucaryotic cells as indicated by its association with ribosomes, its capability to inhibit specifically the cell-free translation of distinct mRNAs, and its interference with the synthesis of two major nucleus-associated proteins in L7 cDNA-transfected Jurkat T-lymphoma cells [F. Neumann et al. (1995) Nucleic Acids Res. 23, 195]. In this report we show that the constitutive expression of protein L7 in Jurkat cells leads to an arrest in G1 of the cell cycle and induces apoptosis as a consequence of cell-to-cell contact. Treatment of the L7 transfectants with the inhibitor of translation cycloheximide, at doses which do not affect untransfected cells, enhances their sensitivity to the induction of apoptosis. These results suggest that L7 can interfere with the translation of proteins which control cell cycle progression and/or the initiation of the apoptotic pathways.

摘要

如蛋白质L7与核糖体的结合、其特异性抑制不同mRNA无细胞翻译的能力以及其对L7 cDNA转染的Jurkat T淋巴瘤细胞中两种主要核相关蛋白合成的干扰所示,蛋白质L7参与真核细胞的翻译控制[F. Neumann等人(1995年)《核酸研究》23,195]。在本报告中,我们表明Jurkat细胞中蛋白质L7的组成型表达导致细胞周期在G1期停滞,并由于细胞间接触而诱导细胞凋亡。用翻译抑制剂环己酰亚胺处理L7转染子,其剂量不影响未转染细胞,可增强它们对凋亡诱导的敏感性。这些结果表明,L7可干扰控制细胞周期进程和/或凋亡途径启动的蛋白质的翻译。

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