• 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

阴性和阳性因素决定了多瘤病毒增强子α结构域在未分化和分化细胞类型中的活性。

Negative and positive factors determine the activity of the polyoma virus enhancer alpha domain in undifferentiated and differentiated cell types.

作者信息

Wasylyk B, Imler J L, Chatton B, Schatz C, Wasylyk C

机构信息

Laboratoire de Génétique Moléculaire des Eucaryotes, l'Institut National de la Santé et de la Recherche Medicale, Faculté de Médecine, Strasbourg, France.

出版信息

Proc Natl Acad Sci U S A. 1988 Nov;85(21):7952-6. doi: 10.1073/pnas.85.21.7952.

DOI:10.1073/pnas.85.21.7952
PMID:2847148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC282331/
Abstract

The host range of polyoma virus is dependent upon the activity of its enhancer, which is inactive in undifferentiated embryonal carcinoma cells, such as F9 cells, and is active after their differentiation. We show here that the activity of the alpha domain of the polyoma virus enhancer displays a similar cell-specificity and inducibility as does the whole enhancer. We present evidence to show that its activity is determined by the balance between the activities of two factors, PEA2, a labile repressor, and PEA1, an inducible positive factor that we have characterized previously. Changes in repressor activity help account for the increase in alpha-domain activity after differentiation of F9 cells. These results suggest that PEA2 is crucial in the regulation of viral gene expression and perhaps more generally in the control of gene expression during differentiation.

摘要

多瘤病毒的宿主范围取决于其增强子的活性,该增强子在未分化的胚胎癌细胞(如F9细胞)中无活性,而在其分化后具有活性。我们在此表明,多瘤病毒增强子α结构域的活性与整个增强子一样,表现出相似的细胞特异性和可诱导性。我们提供证据表明,其活性由两个因子活性之间的平衡决定,即不稳定的阻遏因子PEA2和我们之前已鉴定的可诱导的正因子PEA1。阻遏因子活性的变化有助于解释F9细胞分化后α结构域活性的增加。这些结果表明,PEA2在病毒基因表达的调控中至关重要,或许在更广泛的分化过程中基因表达的控制中也起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/ff8c98984ddc/pnas00300-0134-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/08f0003d6eec/pnas00300-0132-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/46e71c1e0b79/pnas00300-0133-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/0692355a3af2/pnas00300-0133-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/ff8c98984ddc/pnas00300-0134-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/08f0003d6eec/pnas00300-0132-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/46e71c1e0b79/pnas00300-0133-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/0692355a3af2/pnas00300-0133-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d5/282331/ff8c98984ddc/pnas00300-0134-a.jpg

相似文献

1
Negative and positive factors determine the activity of the polyoma virus enhancer alpha domain in undifferentiated and differentiated cell types.阴性和阳性因素决定了多瘤病毒增强子α结构域在未分化和分化细胞类型中的活性。
Proc Natl Acad Sci U S A. 1988 Nov;85(21):7952-6. doi: 10.1073/pnas.85.21.7952.
2
Competition studies with repressors and activators of viral enhancer function in F9 mouse embryonal carcinoma cells.在F9小鼠胚胎癌细胞中对病毒增强子功能的阻遏物和激活物进行的竞争研究。
Nucleic Acids Res. 1987 May 26;15(10):4307-24. doi: 10.1093/nar/15.10.4307.
3
A polyomavirus enhancer-binding protein, PEBP5, responsive to 12-O-tetradecanoylphorbol-13-acetate but distinct from AP-1.一种多瘤病毒增强子结合蛋白,PEBP5,对12-O-十四烷酰佛波醇-13-乙酸酯有反应,但与AP-1不同。
J Virol. 1990 Dec;64(12):5927-38. doi: 10.1128/JVI.64.12.5927-5938.1990.
4
Minimal subenhancer requirements for high-level polyomavirus DNA replication: a cell-specific synergy of PEA3 and PEA1 sites.多瘤病毒DNA高水平复制所需的最小增强子元件:PEA3和PEA1位点的细胞特异性协同作用
Mol Cell Biol. 1990 Sep;10(9):4996-5001. doi: 10.1128/mcb.10.9.4996-5001.1990.
5
A mutated polyoma virus enhancer which is active in undifferentiated embryonal carcinoma cells is not repressed by adenovirus-2 E1A products.一种在未分化胚胎癌细胞中具有活性的突变多瘤病毒增强子不受腺病毒2型E1A产物的抑制。
Nature. 1986;321(6067):249-51. doi: 10.1038/321249a0.
6
Activation of the polyomavirus enhancer by a murine activator protein 1 (AP1) homolog and two contiguous proteins.一种小鼠激活蛋白1(AP1)同源物和两种相邻蛋白对多瘤病毒增强子的激活作用。
Proc Natl Acad Sci U S A. 1988 Aug;85(16):5839-43. doi: 10.1073/pnas.85.16.5839.
7
A tumor promoting phorbol ester, TPA, enhances polyomavirus DNA replication by activating the function of the viral enhancer.一种促肿瘤佛波酯,佛波醇酯(TPA),通过激活病毒增强子的功能来增强多瘤病毒DNA的复制。
Oncogene. 1990 Jan;5(1):5-13.
8
The c-Ha-ras oncogene and a tumor promoter activate the polyoma virus enhancer.c-Ha-ras癌基因和一种肿瘤启动子激活多瘤病毒增强子。
Cell. 1987 Feb 13;48(3):525-34. doi: 10.1016/0092-8674(87)90203-0.
9
Ultraviolet irradiation and c-jun over-expression regulates replication of polyoma sequences in WOP cells through a PEBP2 binding site.
Biochim Biophys Acta. 1995 Mar 14;1261(1):90-8. doi: 10.1016/0167-4781(94)00230-z.
10
A ubiquitous repressor interacting with an F9 cell-specific silencer and its functional suppression by differentiated cell-specific positive factors.一种与F9细胞特异性沉默子相互作用的普遍存在的阻遏物及其被分化细胞特异性阳性因子的功能抑制。
Cell Growth Differ. 1990 Mar;1(3):135-47.

引用本文的文献

1
Inhibition of polyomavirus ori-dependent DNA replication by mSin3B.mSin3B对多瘤病毒ori依赖性DNA复制的抑制作用。
J Virol. 2002 Dec;76(23):11809-18. doi: 10.1128/jvi.76.23.11809-11818.2002.
2
Natural biology of polyomavirus middle T antigen.多瘤病毒中T抗原的自然生物学特性
Microbiol Mol Biol Rev. 2001 Jun;65(2):288-318 ; second and third pages, table of contents. doi: 10.1128/MMBR.65.2.288-318.2001.
3
Competitive binding of viral E2 protein and mammalian core-binding factor to transcriptional control sequences of human papillomavirus type 8 and bovine papillomavirus type 1.

本文引用的文献

1
Isolation and characterization of polyoma virus mutants which grow in murine embryonal carcinoma and trophoblast cells.在小鼠胚胎癌细胞和滋养层细胞中生长的多瘤病毒突变体的分离与鉴定。
EMBO J. 1982;1(12):1521-7. doi: 10.1002/j.1460-2075.1982.tb01349.x.
2
Sequence repeats in a polyoma virus DNA region important for gene expression.多瘤病毒DNA区域中对基因表达重要的序列重复。
J Virol. 1983 Jul;47(1):233-7. doi: 10.1128/JVI.47.1.233-237.1983.
3
Mutation near the polyoma DNA replication origin permits productive infection of F9 embryonal carcinoma cells.
病毒E2蛋白与哺乳动物核心结合因子对人乳头瘤病毒8型和牛乳头瘤病毒1型转录控制序列的竞争性结合。
J Virol. 1997 Oct;71(10):8029-34. doi: 10.1128/JVI.71.10.8029-8034.1997.
4
Characterization of two novel YY1 binding sites in the polyomavirus late promoter.多瘤病毒晚期启动子中两个新型YY1结合位点的表征
J Virol. 1996 Mar;70(3):1433-8. doi: 10.1128/JVI.70.3.1433-1438.1996.
5
Analysis of transcription factors binding to the duplicated PEA1 and PEA3 sites that are required for polyomavirus mutant expression in PCC4 embryonic carcinoma cells.对与多瘤病毒突变体在PCC4胚胎癌细胞中表达所需的重复PEA1和PEA3位点结合的转录因子的分析。
J Virol. 1993 Jun;67(6):3036-47. doi: 10.1128/JVI.67.6.3036-3047.1993.
6
Negative regulation of transcription in eukaryotes.真核生物转录的负调控
Biochem J. 1993 Dec 15;296 ( Pt 3)(Pt 3):521-41. doi: 10.1042/bj2960521.
7
NF-kappa B-independent activation of beta-interferon expression in mouse F9 embryonal carcinoma cells.
Nucleic Acids Res. 1994 Oct 25;22(21):4489-96. doi: 10.1093/nar/22.21.4489.
8
Novel regulation of transcription initiation of the peptide IX gene of adenovirus 2.腺病毒2型肽IX基因转录起始的新型调控
Mol Cell Biol. 1989 Oct;9(10):4265-71. doi: 10.1128/mcb.9.10.4265-4271.1989.
9
Replication-dependent activation of the adenovirus major late promoter is mediated by the increased binding of a transcription factor to sequences in the first intron.腺病毒主要晚期启动子的复制依赖性激活是由转录因子与第一个内含子中的序列结合增加所介导的。
J Virol. 1989 Dec;63(12):5124-32. doi: 10.1128/JVI.63.12.5124-5132.1989.
10
Repression of human cytomegalovirus gene expression associated with a novel immediate early regulatory region binding factor.与一种新型即刻早期调节区结合因子相关的人巨细胞病毒基因表达抑制
Nucleic Acids Res. 1989 Nov 25;17(22):9165-71. doi: 10.1093/nar/17.22.9165.
多瘤病毒DNA复制起点附近的突变允许F9胚胎癌细胞进行有效感染。
Cell. 1981 Mar;23(3):809-14. doi: 10.1016/0092-8674(81)90445-1.
4
Polyoma DNA sequences involved in control of viral gene expression in murine embryonal carcinoma cells.参与小鼠胚胎癌细胞中病毒基因表达调控的多瘤病毒DNA序列。
Nature. 1981 Apr 23;290(5808):720-2. doi: 10.1038/290720a0.
5
Isolation and characterization of polyoma virus mutants able to develop in embryonal carcinoma cells.能够在胚胎癌细胞中生长的多瘤病毒突变体的分离与鉴定。
Proc Natl Acad Sci U S A. 1980 Feb;77(2):1068-72. doi: 10.1073/pnas.77.2.1068.
6
Location of sequences in polyomavirus DNA that are required for early gene expression in vivo and in vitro.多瘤病毒DNA中体内和体外早期基因表达所需序列的定位。
Mol Cell Biol. 1984 Dec;4(12):2594-609. doi: 10.1128/mcb.4.12.2594-2609.1984.
7
Adenovirus-2 E1A products repress enhancer-induced stimulation of transcription.腺病毒2型E1A产物可抑制增强子诱导的转录激活。
Nature. 1984;312(5995):608-12. doi: 10.1038/312608a0.
8
Overlapping positive and negative regulatory domains of the human beta-interferon gene.人类β-干扰素基因的正负调控结构域重叠
Proc Natl Acad Sci U S A. 1988 Mar;85(5):1447-51. doi: 10.1073/pnas.85.5.1447.
9
Oncogene jun encodes a sequence-specific trans-activator similar to AP-1.癌基因jun编码一种与AP-1相似的序列特异性反式激活因子。
Nature. 1988 Mar 10;332(6160):166-71. doi: 10.1038/332166a0.
10
Transforming but not immortalizing oncogenes activate the transcription factor PEA1.转化而非永生化的癌基因激活转录因子PEA1。
EMBO J. 1988 Aug;7(8):2475-83. doi: 10.1002/j.1460-2075.1988.tb03094.x.