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猿猴病毒40起源处选定的RNA聚合酶II启动子元件的复制激活潜力。

The replication activation potential of selected RNA polymerase II promoter elements at the simian virus 40 origin.

作者信息

Hoang A T, Wang W, Gralla J D

机构信息

Department of Chemistry and Biochemistry, University of California, Los Angeles 90024.

出版信息

Mol Cell Biol. 1992 Jul;12(7):3087-93. doi: 10.1128/mcb.12.7.3087-3093.1992.

DOI:10.1128/mcb.12.7.3087-3093.1992
PMID:1320196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC364523/
Abstract

Binding sites for cellular transcription factors were placed near the simian virus 40 origin of replication, and their effect on replication and TATA-dependent transcription was measured in COS cells. The hierarchy of transcriptional stimulation changed when the plasmids replicated. Only one of seven inserted sequences, a moderately weak transcription element, stimulated replication detectably. However, when two nonstimulatory sites were present in multiple copies they did activate replication. Multiple sites for the chimeric activator GAL4-VP16 did not stimulate replication even though transcription was stimulated strongly. The results indicate that the ability of a binding site to stimulate replication from the simian virus 40 ori is not based on its transcriptional activation potential but is instead related to a separate replication activation potential that can be increased by having multiple sites.

摘要

将细胞转录因子的结合位点置于猿猴病毒40复制起点附近,并在COS细胞中测定它们对复制及TATA依赖转录的影响。当质粒复制时,转录刺激的层次发生了变化。七个插入序列中只有一个,即一个中等强度的弱转录元件,能检测到对复制的刺激作用。然而,当两个无刺激作用的位点以多拷贝形式存在时,它们确实能激活复制。嵌合激活因子GAL4-VP16的多个位点即使能强烈刺激转录,也不会刺激复制。结果表明,结合位点刺激猿猴病毒40 ori复制的能力并非基于其转录激活潜力,而是与一种可通过多个位点增加的独立复制激活潜力相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/66baea096a81/molcellb00029-0195-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/55080ec79e19/molcellb00029-0193-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/e348ebd672e4/molcellb00029-0193-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/4296a5e8a8be/molcellb00029-0194-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/fd5383cee9a8/molcellb00029-0194-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/66baea096a81/molcellb00029-0195-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/55080ec79e19/molcellb00029-0193-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/e348ebd672e4/molcellb00029-0193-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/4296a5e8a8be/molcellb00029-0194-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/fd5383cee9a8/molcellb00029-0194-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95d0/364523/66baea096a81/molcellb00029-0195-a.jpg

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引用本文的文献

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Interference of the simian virus 40 origin of replication by the cytomegalovirus immediate early gene enhancer: evidence for competition of active regulatory chromatin conformation in a single domain.巨细胞病毒立即早期基因增强子对猿猴病毒40复制起点的干扰:单一结构域中活性调控染色质构象竞争的证据
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2
Interaction of the transcription factor TFIID with simian virus 40 (SV40) large T antigen interferes with replication of SV40 DNA in vitro.转录因子TFIID与猿猴病毒40(SV40)大T抗原的相互作用会干扰SV40 DNA在体外的复制。
J Virol. 1999 Feb;73(2):1099-107. doi: 10.1128/JVI.73.2.1099-1107.1999.
3

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