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HIV-1反式激活因子调控的新机制与新因子

Novel mechanism and factor for regulation by HIV-1 Tat.

作者信息

Zhou Q, Sharp P A

机构信息

Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.

出版信息

EMBO J. 1995 Jan 16;14(2):321-8. doi: 10.1002/j.1460-2075.1995.tb07006.x.

DOI:10.1002/j.1460-2075.1995.tb07006.x
PMID:7835343
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC398086/
Abstract

Tat regulation of human immunodeficiency virus (HIV) transcription is unique because of its specificity for an RNA target, TAR, and its ability to increase the efficiency of elongation by polymerase. A reconstituted reaction that is Tat-specific and TAR-dependent for activation of HIV transcription has been used to identify and partially purify a cellular activity that is required for trans-activation by Tat, but not by other activators. In the reaction, Tat stimulates the efficiency of elongation by polymerase, whereas Sp1 and other DNA sequence-specific transcription factors activate the rate of initiation. Furthermore, while TATA binding protein (TBP)-associated factors (TAFs) in the TFIID complex are required for activation by transcription factors, they are dispensable for Tat function. Thus, Tat acts through a novel mechanism, which is mediated by a specific host cellular factor, to stimulate HIV-1 gene expression.

摘要

人类免疫缺陷病毒(HIV)转录的Tat调节具有独特性,这是因为它对RNA靶标TAR具有特异性,并且能够提高聚合酶的延伸效率。一种对HIV转录激活具有Tat特异性和TAR依赖性的重组反应已被用于鉴定和部分纯化一种细胞活性,这种活性是Tat反式激活所必需的,但其他激活因子则不需要。在该反应中,Tat刺激聚合酶的延伸效率,而Sp1和其他DNA序列特异性转录因子激活起始速率。此外,虽然TFIID复合物中的TATA结合蛋白(TBP)相关因子(TAFs)是转录因子激活所必需的,但它们对于Tat功能是可有可无的。因此,Tat通过一种由特定宿主细胞因子介导的新机制来刺激HIV-1基因表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/e95b890aae2e/emboj00026-0128-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/34078de318f2/emboj00026-0124-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/c62c4dc4b915/emboj00026-0125-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/fb0e85b0f28d/emboj00026-0125-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/2c9d29e19eec/emboj00026-0126-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/584147dc9fad/emboj00026-0127-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/e95b890aae2e/emboj00026-0128-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/34078de318f2/emboj00026-0124-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/c62c4dc4b915/emboj00026-0125-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/fb0e85b0f28d/emboj00026-0125-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/2c9d29e19eec/emboj00026-0126-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/584147dc9fad/emboj00026-0127-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/398086/e95b890aae2e/emboj00026-0128-a.jpg

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Does HIV-1 Tat induce a change in viral initiation rights?HIV-1反式激活因子(Tat)是否会引起病毒起始权的变化?
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The human immunodeficiency virus type 1 long terminal repeat specifies two different transcription complexes, only one of which is regulated by Tat.
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