Tumor necrosis factor-alpha induces a kappa B sequence-specific DNA-binding protein in human hepatoblastoma HepG2 cells.
Tumor necrosis factor-alpha induces a kappa B sequence-specific DNA-binding protein in human hepatoblastoma HepG2 cells.
复制标题
肿瘤坏死因子-α 在人肝母细胞瘤 HepG2 细胞中诱导 kappa B 序列特异性 DNA 结合蛋白。
DOI：
10.1002/hep.1840100620
复制
发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Acs,G
中科院分区：
文献类型：
--
作者：
Banerjee,R;Karpen,S;Siekevitz,M;Lengyel,G;Bauer,J;Acs,G
肿瘤坏死因子-α 是肝细胞中急性期蛋白质合成的诱导剂。肿瘤坏死因子-α 改变这些细胞中基因表达的机制在很大程度上尚不清楚。在这项研究中，我们证明肿瘤坏死因子-α 刺激人类免疫缺陷病毒-1 长末端重复序列促进人肝母细胞瘤 HepG2 细胞系中的基因表达，并增加反式激活因子与 kappa B (k B) DNA 序列的结合。淋巴细胞中识别 k B 序列的核因子通过翻译后机制被肿瘤坏死因子 -α 和佛波醇 - 12 - 肉豆蔻酸 - 13 - 乙酸盐激活，而在 HepG2 细胞中，佛波醇 - 12 - 肉豆蔻酸 - 13 - 乙酸盐不会激活这些因子，并且 HepG2 细胞似乎需要从头合成蛋白质 用于肿瘤坏死因子-α 的基因激活。
Tumor necrosis factor–α is an inducer of acute–phase protein synthesis in liver cells. The mechanism by which tumor necrosis factor–α alters gene expression in these cells is largely unknown. In this study, we demonstrate that tumor necrosis factor–α stimulates human immunodeficiency virus–1 long terminal repeat–promoted gene expression in the human hepatoblastoma HepG2 cell line and increased binding of trans–activating factors to kappa B (k B) DNA sequences. In contrast to lymphocytic cells where the nuclear factors recognizing the k B sequences are activated by both tumor necrosis factor–α and phorbol–12–myristate–13–acetate through a posttranslational mechanism, in HepG2 cells phorbol–12–myristate–13–acetate does not activate these factor (s), and de novo protein synthesis seems to be required in HepG2 cells for gene activation by tumor necrosis factor–α.