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由c-jun和激活的c-Ha-ras癌基因诱导的F9胚胎癌细胞分化

Differentiation of F9 embryonal carcinoma cells induced by the c-jun and activated c-Ha-ras oncogenes.

作者信息

Yamaguchi-Iwai Y, Satake M, Murakami Y, Sakai M, Muramatsu M, Ito Y

机构信息

Department of Viral Oncology, Kyoto University, Japan.

出版信息

Proc Natl Acad Sci U S A. 1990 Nov;87(21):8670-4. doi: 10.1073/pnas.87.21.8670.

DOI:10.1073/pnas.87.21.8670
PMID:2122465
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC55019/
Abstract

The activated c-Ha-ras oncogene induced AP1-site DNA-binding activity in F9 cells. This induction appeared to be due, at least in part, to the induction of c-jun transcription. Both activated c-Ha-ras and c-jun induced the differentiation of F9 cells to endoderm-like cells. Thus, AP1 appears to play a key role in the initial stage of F9 cell differentiation.

摘要

活化的c-Ha-ras癌基因在F9细胞中诱导了AP1位点的DNA结合活性。这种诱导作用似乎至少部分归因于c-jun转录的诱导。活化的c-Ha-ras和c-jun均诱导F9细胞分化为内胚层样细胞。因此,AP1似乎在F9细胞分化的初始阶段起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/4fc31d2997f8/pnas01046-0496-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/988634102d32/pnas01046-0494-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/82bffb79dac5/pnas01046-0495-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/f2d23c5fc7a6/pnas01046-0495-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/884228acf8cd/pnas01046-0496-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/fe7666e0abe7/pnas01046-0496-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/2c064803cad8/pnas01046-0496-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/4fc31d2997f8/pnas01046-0496-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/988634102d32/pnas01046-0494-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/82bffb79dac5/pnas01046-0495-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/f2d23c5fc7a6/pnas01046-0495-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/884228acf8cd/pnas01046-0496-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/fe7666e0abe7/pnas01046-0496-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/2c064803cad8/pnas01046-0496-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1290/55019/4fc31d2997f8/pnas01046-0496-d.jpg

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Differentiation of F9 embryonal carcinoma cells induced by the c-jun and activated c-Ha-ras oncogenes.由c-jun和激活的c-Ha-ras癌基因诱导的F9胚胎癌细胞分化
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2
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JDP2, a repressor of AP-1, recruits a histone deacetylase 3 complex to inhibit the retinoic acid-induced differentiation of F9 cells.

本文引用的文献

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T24 human bladder carcinoma oncogene is an activated form of the normal human homologue of BALB- and Harvey-MSV transforming genes.
JDP2是AP-1的一种阻遏物,它募集一种组蛋白去乙酰化酶3复合物以抑制视黄酸诱导的F9细胞分化。
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Mouse actin messenger RNAs. Construction and characterization of a recombinant plasmid molecule containing a complementary DNA transcript of mouse alpha-actin mRNA.小鼠肌动蛋白信使核糖核酸。含有小鼠α-肌动蛋白信使核糖核酸互补脱氧核糖核酸转录物的重组质粒分子的构建与特性分析。
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Teratocarcinomas and mammalian embryogenesis.畸胎癌与哺乳动物胚胎发育
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Cell. 1988 Dec 2;55(5):917-24. doi: 10.1016/0092-8674(88)90147-x.
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Fos and Jun: the AP-1 connection.Fos与Jun:AP-1连接
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