• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

未分化的OTF963胚胎癌细胞早期感染期间腺病毒基因的表达缺陷。

Defective expression of adenovirus genes during early infection of undifferentiated OTF963 embryonal carcinoma cells.

作者信息

Nelson C C, Braithwaite A W, Silvestro M, Bellett A J

机构信息

Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra.

出版信息

J Virol. 1990 Sep;64(9):4329-37. doi: 10.1128/JVI.64.9.4329-4337.1990.

DOI:10.1128/JVI.64.9.4329-4337.1990
PMID:2143541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC247900/
Abstract

Adenovirus infection was compared in F9 (OTF963) cells and cells induced to differentiate with retinoic acid, in order to study expression of early genes under the control of the reported "E1a-like factor" in F9 cells. However, not only was transcription of the viral E1a gene defective in undifferentiated cells but expression of all the other early genes was found to be reduced in OTF963 cells in comparison to differentiated cells. The defect in early gene expression was detected at the level of transcriptional initiation during the first 48 h of infection and resulted in similarly low levels of viral cytoplasmic mRNA and viral protein synthesis. Viral DNA replication was delayed and reduced. After 48 h of infection, the defect in transcription in OTF963 cells of E1a and other early genes was relieved, so that by 72 h postinfection the level of transcription was similar to that 16 h after infection of differentiated cells. At no time did adenovirus early gene expression occur independently of viral E1a. These results suggest limits to the generality and explanatory power of the hypothesis that F9 embryonal carcinoma cells contain an E1a-like factor.

摘要

为了研究F9(OTF963)细胞中在已报道的“E1a样因子”控制下早期基因的表达情况,对F9(OTF963)细胞和用视黄酸诱导分化的细胞中的腺病毒感染进行了比较。然而,不仅未分化细胞中病毒E1a基因的转录存在缺陷,而且与分化细胞相比,OTF963细胞中所有其他早期基因的表达也被发现有所降低。在感染的最初48小时内,早期基因表达的缺陷在转录起始水平被检测到,导致病毒细胞质mRNA和病毒蛋白合成水平同样较低。病毒DNA复制延迟且减少。感染48小时后,OTF963细胞中E1a和其他早期基因转录的缺陷得到缓解,因此到感染后72小时,转录水平与分化细胞感染16小时后的水平相似。腺病毒早期基因表达在任何时候都不会独立于病毒E1a发生。这些结果表明,F9胚胎癌细胞含有E1a样因子这一假说的普遍性和解释力存在局限性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/10f9456ce540/jvirol00064-0306-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/d3f7e9626e26/jvirol00064-0303-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/cd2f62ad21e5/jvirol00064-0304-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/c1e0e23b9141/jvirol00064-0305-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/3880310ad96d/jvirol00064-0305-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/10f9456ce540/jvirol00064-0306-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/d3f7e9626e26/jvirol00064-0303-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/cd2f62ad21e5/jvirol00064-0304-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/c1e0e23b9141/jvirol00064-0305-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/3880310ad96d/jvirol00064-0305-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a1/247900/10f9456ce540/jvirol00064-0306-a.jpg

相似文献

1
Defective expression of adenovirus genes during early infection of undifferentiated OTF963 embryonal carcinoma cells.未分化的OTF963胚胎癌细胞早期感染期间腺病毒基因的表达缺陷。
J Virol. 1990 Sep;64(9):4329-37. doi: 10.1128/JVI.64.9.4329-4337.1990.
2
E1a-dependent expression of adenovirus genes in OTF963 embryonal carcinoma cells: role of E1a-induced differentiation.腺病毒基因在OTF963胚胎癌细胞中E1a依赖性表达:E1a诱导分化的作用
Proc Natl Acad Sci U S A. 1990 Oct;87(20):8041-5. doi: 10.1073/pnas.87.20.8041.
3
Developmental control of a promoter-specific factor that is also regulated by the E1A gene product.
Cell. 1987 Feb 13;48(3):501-6. doi: 10.1016/0092-8674(87)90200-5.
4
The state of cellular differentiation determines the activity of the adenovirus E1A enhancer element: evidence for negative regulation of enhancer function.细胞分化状态决定腺病毒E1A增强子元件的活性:增强子功能负调控的证据。
J Virol. 1990 Jan;64(1):161-72. doi: 10.1128/JVI.64.1.161-172.1990.
5
Adenovirus infection of differentiated F9 cells results in a global shut-off of differentiation-induced gene expression.分化的F9细胞感染腺病毒会导致分化诱导基因表达全面关闭。
Nucleic Acids Res. 1990 Oct 25;18(20):6107-12. doi: 10.1093/nar/18.20.6107.
6
Sequence-independent autoregulation of the adenovirus type 5 E1A transcription unit.5型腺病毒E1A转录单元的序列非依赖性自调控
Mol Cell Biol. 1985 Nov;5(11):3214-21. doi: 10.1128/mcb.5.11.3214-3221.1985.
7
An insertion mutation in the adenovirus type 12 early region 1A 13S mRNA unique region.腺病毒12型早期区域1A 13S信使核糖核酸独特区域的插入突变。
J Virol. 1986 Feb;57(2):490-6. doi: 10.1128/JVI.57.2.490-496.1986.
8
Transcriptional regulation of the c-jun gene by retinoic acid and E1A during differentiation of F9 cells.维甲酸和E1A在F9细胞分化过程中对c-jun基因的转录调控。
EMBO J. 1992 Jan;11(1):167-75. doi: 10.1002/j.1460-2075.1992.tb05039.x.
9
Adenovirus 12S E1A gene represses differentiation of F9 teratocarcinoma cells.腺病毒12S E1A基因抑制F9畸胎瘤细胞的分化。
Proc Natl Acad Sci U S A. 1990 Dec;87(24):9878-82. doi: 10.1073/pnas.87.24.9878.
10
Adenovirus E1A and E1B genes are regulated posttranscriptionally in human lymphoid cells.腺病毒E1A和E1B基因在人类淋巴细胞中受到转录后调控。
J Virol. 1990 Nov;64(11):5349-59. doi: 10.1128/JVI.64.11.5349-5359.1990.

引用本文的文献

1
Convergent regulation of NF-IL6 and Oct-1 synthesis by interleukin-6 and retinoic acid signaling in embryonal carcinoma cells.胚胎癌细胞中白细胞介素-6和视黄酸信号对NF-IL6和Oct-1合成的趋同调节。
Mol Cell Biol. 1993 Apr;13(4):2515-23. doi: 10.1128/mcb.13.4.2515-2523.1993.
2
E1a-dependent expression of adenovirus genes in OTF963 embryonal carcinoma cells: role of E1a-induced differentiation.腺病毒基因在OTF963胚胎癌细胞中E1a依赖性表达:E1a诱导分化的作用
Proc Natl Acad Sci U S A. 1990 Oct;87(20):8041-5. doi: 10.1073/pnas.87.20.8041.

本文引用的文献

1
Early viral proteins in HeLa cells infected with adenovirus type 5 host range mutants.感染5型腺病毒宿主范围突变体的HeLa细胞中的早期病毒蛋白。
Virology. 1980 Jun;103(2):475-92. doi: 10.1016/0042-6822(80)90205-6.
2
Mechanism of activation of early viral transcription by the adenovirus E1A gene product.腺病毒E1A基因产物激活早期病毒转录的机制。
Cell. 1981 Oct;26(2 Pt 2):213-20. doi: 10.1016/0092-8674(81)90304-4.
3
Retinoic acid-induced differentiation of F9 embryonal carcinoma cells.维甲酸诱导F9胚胎癌细胞分化。
Exp Cell Res. 1981 Apr;132(2):453-60. doi: 10.1016/0014-4827(81)90120-8.
4
Regulation of type 5 adenovirus replication in murine teratocarcinoma cell lines.
Virology. 1982 Nov;123(1):45-59. doi: 10.1016/0042-6822(82)90293-8.
5
Cell-cycle characteristics of undifferentiated and differentiating embryonal carcinoma cells.
Dev Biol. 1982 Feb;89(2):516-20. doi: 10.1016/0012-1606(82)90340-2.
6
Transcriptional activation and subsequent control of the human heat shock gene during adenovirus infection.腺病毒感染期间人类热休克基因的转录激活及后续调控。
Mol Cell Biol. 1983 Nov;3(11):2058-65. doi: 10.1128/mcb.3.11.2058-2065.1983.
7
Common control of the heat shock gene and early adenovirus genes: evidence for a cellular E1A-like activity.热休克基因与早期腺病毒基因的共同调控:细胞中类似E1A活性的证据。
Mol Cell Biol. 1984 May;4(5):867-74. doi: 10.1128/mcb.4.5.867-874.1984.
8
Non-function of a Moloney murine leukaemia virus regulatory sequence in F9 embryonal carcinoma cells.莫洛尼鼠白血病病毒调控序列在F9胚胎癌细胞中的无功能状态
Nature. 1984;308(5958):470-2. doi: 10.1038/308470a0.
9
The interaction of polyoma virus with F9 embryonal carcinoma cells and chemically induced differentiated progeny: fate of the viral DNA and expression of viral antigens.
J Cell Physiol Suppl. 1982;2:69-83. doi: 10.1002/jcp.1041130512.
10
Delayed de novo methylation in teratocarcinoma suggests additional tissue-specific mechanisms for controlling gene expression.畸胎癌中的延迟从头甲基化表明存在控制基因表达的其他组织特异性机制。
Nature. 1983 Jan 6;301(5895):32-7. doi: 10.1038/301032a0.