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短转录本诱导因子的特性分析,一种激活短RNA合成的人类免疫缺陷病毒1型转录元件。

Characterization of the inducer of short transcripts, a human immunodeficiency virus type 1 transcriptional element that activates the synthesis of short RNAs.

作者信息

Sheldon M, Ratnasabapathy R, Hernandez N

机构信息

Cold Spring Harbor Laboratory, New York 11724.

出版信息

Mol Cell Biol. 1993 Feb;13(2):1251-63. doi: 10.1128/mcb.13.2.1251-1263.1993.

DOI:10.1128/mcb.13.2.1251-1263.1993
PMID:8423790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC359010/
Abstract

The inducer of short transcripts, or IST, is an unusual transcriptional element located downstream of the human immunodeficiency virus type 1 (HIV-1) promoter. IST activates HIV-1 transcription, but the resulting RNAs are short and end at approximately position +59. IST, therefore, appears to promote the formation of transcription complexes that are unable to elongate efficiently. This activity contrasts with that of TAR, the target for Tat trans-activation, which upon binding of the viral protein Tat promotes the formation of transcription complexes capable of efficient elongation through the entire viral genome. We have localized and characterized the IST element. Our results indicate that IST is located mainly between positions -5 and +26, although the sequences from positions +40 to +59 also contribute to IST activity. Unlike TAR, which is an RNA element, IST appears to be a DNA element. Thus, the HIV-1 R region is a complex regulatory region with RNA and DNA elements that promote the formation of transcription complexes with different elongation properties.

摘要

短转录本诱导子(IST)是位于人类免疫缺陷病毒1型(HIV-1)启动子下游的一种特殊转录元件。IST可激活HIV-1转录,但产生的RNA较短,终止于大约+59位。因此,IST似乎促进了无法有效延伸的转录复合物的形成。这种活性与Tat反式激活的靶标TAR的活性相反,TAR在病毒蛋白Tat结合后,促进能够有效延伸通过整个病毒基因组的转录复合物的形成。我们已经对IST元件进行了定位和表征。我们的结果表明,IST主要位于-5至+26位之间,尽管+40至+59位的序列也对IST活性有贡献。与作为RNA元件的TAR不同,IST似乎是一种DNA元件。因此,HIV-1 R区域是一个复杂的调控区域,含有RNA和DNA元件,它们促进形成具有不同延伸特性的转录复合物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/72cc5392d6d9/molcellb00014-0544-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/02db0ee59c7d/molcellb00014-0538-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/f649e14437c1/molcellb00014-0540-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/0d5912eaffda/molcellb00014-0542-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/72cc5392d6d9/molcellb00014-0544-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/02db0ee59c7d/molcellb00014-0538-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/f649e14437c1/molcellb00014-0540-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/0d5912eaffda/molcellb00014-0542-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fb5/359010/72cc5392d6d9/molcellb00014-0544-a.jpg

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