Electroporation and carrier DNA cause p53 activation, cell cycle arrest, and apoptosis
Electroporation and carrier DNA cause p53 activation, cell cycle arrest, and apoptosis
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DOI：
10.1016/s0003-2697(03)00135-0
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发表时间：
2003-07-01
影响因子：
2.9
通讯作者：
Maimets, T
中科院分区：
文献类型：
--
作者：
Lepik, D;Jaks, V;Maimets, T
用于瞬时转染细胞的方法可能改变细胞信号传导途径，这反过来可能导致对结果的误解。多种遗传毒性剂引起p53蛋白的积累，导致细胞凋亡或生长停滞。在这里，我们报告的电穿孔和载体DNA的稳定性，细胞定位和转录活性的p53的影响。我们发现，电穿孔导致p53依赖性和p53非依赖性细胞周期阻滞和凋亡。同时，也用于瞬时转染细胞的化学试剂聚乙烯亚胺既不引起p53的上调也不引起细胞应答。(C)2003 Elsevier Science（美国）。All rights reserved.
Methods used in transient transfection of cells may alter cellular signaling pathways that in turn may lead to misinterpretation of the results. A variety of genotoxic agents cause the accumulation of the p53 protein leading to either apoptosis or growth arrest. Here we report the effect of electroporation and carrier DNA on the stability, cellular localization, and transcriptional activity of p53. We show that electroporation leads to p53-dependent and also p53-independent cell-cycle arrest and apoptosis. At the same time a chemical agent polyethylenimine that is also used for transient transfection of cells causes neither upregulation of p53 nor cellular response. (C) 2003 Elsevier Science (USA). All rights reserved.