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腺病毒5型12S E1a蛋白而非13S蛋白可诱导F9细胞中endoA分化标志物的表达。

The adenovirus-5 12S E1a protein, but not the 13S induces expression of the endoA differentiation marker in F9 cells.

作者信息

Velcich A, Ziff E B

机构信息

Department of Biochemistry, New York University School of Medicine, NY 10016.

出版信息

Oncogene. 1989 Jun;4(6):707-13.

PMID:2543941
Abstract

F9 embryonal carcinoma (EC) cells serve as a model system for early mammalian development. We have investigated the effect of the E1a gene products on the F9 cell differentiation program by stably introducing into these cells plasmids which express wild type or mutant forms of E1a. We have found that expression of the 12S E1a mRNA product results in the expression of the endoA gene, a marker specific for the differentiated phenotype of F9 cells, as well as an altered cell morphology associated with the differentiated state. These alterations are not observed in F9 cells which express the 13S E1a product. Other markers specific for the differentiated state are regulated normally in the E1a transformants following exposure to retinoic acid (R.A.) and dibutyryl cyclic AMP (dbcAMP). We discuss these results in the context of the well established transcriptional activities of the E1a proteins.

摘要

F9胚胎癌细胞系是早期哺乳动物发育的模型系统。我们通过稳定地将表达野生型或突变型E1a的质粒导入这些细胞,研究了E1a基因产物对F9细胞分化程序的影响。我们发现,12S E1a mRNA产物的表达导致endoA基因的表达,endoA基因是F9细胞分化表型的特异性标志物,同时还伴有与分化状态相关的细胞形态改变。在表达13S E1a产物的F9细胞中未观察到这些改变。在暴露于视黄酸(R.A.)和二丁酰环磷酸腺苷(dbcAMP)后,E1a转化体中其他分化状态特异性标志物的调控正常。我们结合E1a蛋白已确定的转录活性来讨论这些结果。

相似文献

1
The adenovirus-5 12S E1a protein, but not the 13S induces expression of the endoA differentiation marker in F9 cells.腺病毒5型12S E1a蛋白而非13S蛋白可诱导F9细胞中endoA分化标志物的表达。
Oncogene. 1989 Jun;4(6):707-13.
2
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E1a-dependent expression of adenovirus genes in OTF963 embryonal carcinoma cells: role of E1a-induced differentiation.
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Functional analysis of an isolated fos promoter element with AP-1 site homology reveals cell type-specific transcriptional properties.对具有AP-1位点同源性的分离的fos启动子元件进行功能分析,揭示了细胞类型特异性转录特性。
Mol Cell Biol. 1990 Dec;10(12):6273-82. doi: 10.1128/mcb.10.12.6273-6282.1990.
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