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J Virol. 1999 Dec;73(12):10254-63. doi: 10.1128/JVI.73.12.10254-10263.1999.
2
Murine polyomavirus and simian virus 40 large T antigens produce different structural alterations in viral origin DNA.鼠多瘤病毒和猿猴病毒40大T抗原在病毒起源DNA中产生不同的结构改变。
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A model for the T-antigen-induced structural alteration of the SV40 replication origin based upon experiments with specific probes for bent, straight, and unwound DNA.基于针对弯曲、直线和解旋DNA的特异性探针实验得出的T抗原诱导SV40复制起点结构改变的模型。
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本文引用的文献

1
The activity of topoisomerase I is modulated by large T antigen during unwinding of the SV40 origin.在SV40起始点解旋过程中,拓扑异构酶I的活性受大T抗原调控。
J Biol Chem. 1998 Aug 7;273(32):20390-6. doi: 10.1074/jbc.273.32.20390.
2
The initiation of simian virus 40 DNA replication in vitro.猿猴病毒40 DNA在体外的复制起始
Crit Rev Biochem Mol Biol. 1997;32(6):503-68. doi: 10.3109/10409239709082001.
3
TBP binding to the TATA box induces a specific downstream unwinding site that is targeted by pluramycin.TBP与TATA盒结合会诱导一个特定的下游解旋位点,该位点是嘌呤霉素的作用靶点。
Chem Biol. 1995 Jul;2(7):457-69. doi: 10.1016/1074-5521(95)90263-5.
4
Dimerization of simian virus 40 T-antigen hexamers activates T-antigen DNA helicase activity.猿猴病毒40 T抗原六聚体的二聚化激活了T抗原DNA解旋酶活性。
J Virol. 1997 Nov;71(11):8766-73. doi: 10.1128/JVI.71.11.8766-8773.1997.
5
Functional equivalency and diversity of cis-acting elements among yeast replication origins.酵母复制起点间顺式作用元件的功能等效性与多样性
Mol Cell Biol. 1997 Sep;17(9):5473-84. doi: 10.1128/MCB.17.9.5473.
6
Simian virus 40 large T antigen binds to topoisomerase I.猴病毒40大T抗原与拓扑异构酶I结合。
Virology. 1996 Aug 15;222(2):365-74. doi: 10.1006/viro.1996.0433.
7
A model for the T-antigen-induced structural alteration of the SV40 replication origin based upon experiments with specific probes for bent, straight, and unwound DNA.基于针对弯曲、直线和解旋DNA的特异性探针实验得出的T抗原诱导SV40复制起点结构改变的模型。
Biochemistry. 1996 Jun 18;35(24):7993-8001. doi: 10.1021/bi960251d.
8
An N-terminal deletion mutant of simian virus 40 (SV40) large T antigen oligomerizes incorrectly on SV40 DNA but retains the ability to bind to DNA polymerase alpha and replicate SV40 DNA in vitro.猿猴病毒40(SV40)大T抗原的N端缺失突变体在SV40 DNA上错误地寡聚,但保留了与DNA聚合酶α结合并在体外复制SV40 DNA的能力。
J Virol. 1996 Jun;70(6):3509-16. doi: 10.1128/JVI.70.6.3509-3516.1996.
9
(+)-CC-1065 as a structural probe of Mu transposase-induced bending of DNA: overcoming limitations of hydroxyl-radical footprinting.
Nucleic Acids Res. 1993 Sep 11;21(18):4281-7. doi: 10.1093/nar/21.18.4281.
10
The DNA-binding domain of simian virus 40 tumor antigen has multiple functions.猿猴病毒40肿瘤抗原的DNA结合结构域具有多种功能。
J Virol. 1993 Dec;67(12):7608-11. doi: 10.1128/JVI.67.12.7608-7611.1993.

猴病毒40重排调控区的构象变化:21个碱基对启动子的作用及其位置

Conformational changes in simian virus 40 rearranged regulatory regions: effects of the 21-base-pair promoters and their location.

作者信息

Wilderman P J, Hu B, Woodworth M E

机构信息

Department of Microbiology, Miami University, Oxford, Ohio 45056, USA.

出版信息

J Virol. 1999 Dec;73(12):10254-63. doi: 10.1128/JVI.73.12.10254-10263.1999.

DOI:10.1128/JVI.73.12.10254-10263.1999
PMID:10559342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC113079/
Abstract

Simian virus 40 (SV40) is an excellent model system for investigating the cis- and trans-acting factors involved in eukaryotic DNA replication because it uses host enzymes, with the exception of the virus-encoded T-antigen (T-ag), to replicate its genome. Although its origin of replication (ori) is essential for DNA replication, there are transcriptional promoters and enhancers that affect DNA replication efficiency. T-ag binds to sites I to III within and around ori with different affinities and induces structural changes. We were interested in determining if the position of the promoters relative to ori influences the binding of T-ag to these regions. Furthermore, we characterized the DNA structural changes that occur as a result of protein binding when the promoters are absent and also when the promoters are moved from their wild-type position upstream of ori to a position downstream of ori. Using sequence- and conformation-specific chemical probes, our data indicate that (i) the conformation of site I is influenced by T-ag binding and by flanking sequences, (ii) the conformation of the promoters after T-ag binding is dependent on their location, and (iii) unwinding of ori is influenced by the location of the promoters and their presence or absence. These differences in DNA conformation may help explain decreases in relative DNA replication efficiency that occur when the promoters are absent or located downstream of ori.

摘要

猴病毒40(SV40)是研究真核生物DNA复制中顺式和反式作用因子的优秀模型系统,因为它除了病毒编码的T抗原(T-ag)外,利用宿主酶来复制其基因组。尽管其复制起点(ori)对DNA复制至关重要,但也存在影响DNA复制效率的转录启动子和增强子。T-ag以不同亲和力结合到ori内部及周围的位点I至III,并诱导结构变化。我们感兴趣的是确定启动子相对于ori的位置是否会影响T-ag与这些区域的结合。此外,我们还对在没有启动子以及将启动子从ori上游的野生型位置移至ori下游位置时,由于蛋白质结合而发生的DNA结构变化进行了表征。使用序列和构象特异性化学探针,我们的数据表明:(i)位点I的构象受T-ag结合和侧翼序列的影响;(ii)T-ag结合后启动子的构象取决于其位置;(iii)ori的解旋受启动子位置及其存在与否的影响。DNA构象的这些差异可能有助于解释在没有启动子或启动子位于ori下游时相对DNA复制效率的降低。