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本文引用的文献

1
Adenovirus E4orf6 targets pp32/LANP to control the fate of ARE-containing mRNAs by perturbing the CRM1-dependent mechanism.腺病毒E4orf6靶向pp32/LANP,通过干扰依赖CRM1的机制来控制含ARE的mRNA的命运。
J Cell Biol. 2005 Jul 4;170(1):15-20. doi: 10.1083/jcb.200405112. Epub 2005 Jun 27.
2
Interaction of the adenovirus major core protein precursor, pVII, with the viral DNA packaging machinery.腺病毒主要核心蛋白前体pVII与病毒DNA包装机制的相互作用。
Virology. 2005 Apr 10;334(2):194-202. doi: 10.1016/j.virol.2005.01.048.
3
Adenovirus protein VII functions throughout early phase and interacts with cellular proteins SET and pp32.腺病毒蛋白VII在整个早期阶段发挥作用,并与细胞蛋白SET和pp32相互作用。
J Virol. 2005 Feb;79(4):2474-83. doi: 10.1128/JVI.79.4.2474-2483.2005.
4
The histone chaperone TAF-I/SET/INHAT is required for transcription in vitro of chromatin templates.组蛋白伴侣TAF-I/SET/INHAT是染色质模板体外转录所必需的。
Mol Cell Biol. 2005 Jan;25(2):797-807. doi: 10.1128/MCB.25.2.797-807.2005.
5
Adenovirus protein VII condenses DNA, represses transcription, and associates with transcriptional activator E1A.腺病毒蛋白VII使DNA浓缩,抑制转录,并与转录激活因子E1A结合。
J Virol. 2004 Jun;78(12):6459-68. doi: 10.1128/JVI.78.12.6459-6468.2004.
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Strategies for generation of an siRNA expression library directed against the human genome.针对人类基因组生成小干扰RNA表达文库的策略。
Oligonucleotides. 2003;13(5):325-33. doi: 10.1089/154545703322617005.
7
Ternary complex formation between DNA-adenovirus core protein VII and TAF-Ibeta/SET, an acidic molecular chaperone.DNA - 腺病毒核心蛋白VII与TAF - Iβ/SET(一种酸性分子伴侣)之间三元复合物的形成。
FEBS Lett. 2003 Dec 18;555(3):521-7. doi: 10.1016/s0014-5793(03)01336-x.
8
Herpes simplex virus type 1 tegument protein VP22 interacts with TAF-I proteins and inhibits nucleosome assembly but not regulation of histone acetylation by INHAT.单纯疱疹病毒1型被膜蛋白VP22与TAF-I蛋白相互作用,并抑制核小体组装,但不抑制INHAT对组蛋白乙酰化的调控。
J Gen Virol. 2003 Sep;84(Pt 9):2501-2510. doi: 10.1099/vir.0.19326-0.
9
Adenovirus type 5 DNA-protein complexes from formaldehyde cross-linked cells early after infection.感染后早期来自甲醛交联细胞的5型腺病毒DNA-蛋白质复合物。
Virology. 2003 Jul 20;312(1):204-12. doi: 10.1016/s0042-6822(03)00194-6.
10
Import of adenovirus DNA involves the nuclear pore complex receptor CAN/Nup214 and histone H1.腺病毒DNA的导入涉及核孔复合体受体CAN/Nup214和组蛋白H1。
Nat Cell Biol. 2001 Dec;3(12):1092-100. doi: 10.1038/ncb1201-1092.

模板激活因子I/SET作为一种正性作用因子参与腺病毒早期基因的转录。

Involvement of template-activating factor I/SET in transcription of adenovirus early genes as a positive-acting factor.

作者信息

Haruki Hirohito, Okuwaki Mitsuru, Miyagishi Makoto, Taira Kazunari, Nagata Kyosuke

机构信息

Department of Infection Biology, Graduate School of Comprehensive Human Sciences and Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8575, Japan.

出版信息

J Virol. 2006 Jan;80(2):794-801. doi: 10.1128/JVI.80.2.794-801.2006.

DOI:10.1128/JVI.80.2.794-801.2006
PMID:16378981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1346848/
Abstract

The adenovirus genome complexed with viral core protein VII (adenovirus DNA-protein VII complex) at least is the bona fide template for transcription of adenovirus early genes. It is believed that the highly basic protein VII, like cellular histones, is a negative regulator for genome functions. Analyses with in vitro replication and transcription systems using the adenovirus DNA-protein VII complex have revealed that remodeling of the complex is crucial for efficient DNA replication and transcription. We identified host acidic proteins, template-activating factor I (TAF-I), TAF-II, and TAF-III as stimulatory factors for replication from the adenovirus DNA-protein VII complex. Recently, it was reported that the adenovirus DNA interacts with TAF-I and pp32, another host acidic protein (Y. Xue, J. S. Johnson, D. A. Ornelles, J. Lieberman, and D. A. Engel, J. Virol. 79:2474-2483, 2005). We found that TAF-I interacts and colocalizes with protein VII in adenovirus-infected cells during the early phases of infection, but pp32 does not. Although pp32 had the potential ability to interact with protein VII, pp32 did not remodel the adenovirus DNA-protein VII complex in vitro. Small interfering RNA-mediated knockdown of TAF-I expression leads to the delay of the transcription timing of early genes. These results provide evidence that TAF-I plays an important role in the early stages of the adenovirus infection cycle.

摘要

与病毒核心蛋白VII复合的腺病毒基因组(腺病毒DNA-蛋白VII复合物)至少是腺病毒早期基因转录的真正模板。据信,高度碱性的蛋白VII与细胞组蛋白一样,是基因组功能的负调节因子。使用腺病毒DNA-蛋白VII复合物的体外复制和转录系统分析表明,该复合物的重塑对于有效的DNA复制和转录至关重要。我们鉴定出宿主酸性蛋白模板激活因子I(TAF-I)、TAF-II和TAF-III是腺病毒DNA-蛋白VII复合物复制的刺激因子。最近,有报道称腺病毒DNA与TAF-I和另一种宿主酸性蛋白pp32相互作用(Y. Xue、J. S. Johnson、D. A. Ornelles、J. Lieberman和D. A. Engel,《病毒学杂志》79:2474-2483,2005年)。我们发现,在感染早期,TAF-I在腺病毒感染细胞中与蛋白VII相互作用并共定位,但pp32并非如此。尽管pp32具有与蛋白VII相互作用的潜在能力,但pp32在体外并未重塑腺病毒DNA-蛋白VII复合物。小干扰RNA介导的TAF-I表达敲低导致早期基因转录时间延迟。这些结果证明TAF-I在腺病毒感染周期的早期阶段发挥重要作用。