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人类嗜T淋巴细胞病毒1型(HTLV-1)的转录后调节因子(rex)启动病毒结构蛋白的表达,但抑制调节蛋白的表达。

Post-transcriptional regulator (rex) of HTLV-1 initiates expression of viral structural proteins but suppresses expression of regulatory proteins.

作者信息

Hidaka M, Inoue J, Yoshida M, Seiki M

机构信息

Department of Viral Oncology, Cancer Institute, Tokyo, Japan.

出版信息

EMBO J. 1988 Feb;7(2):519-23. doi: 10.1002/j.1460-2075.1988.tb02840.x.

DOI:10.1002/j.1460-2075.1988.tb02840.x
PMID:2835230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC454349/
Abstract

Gene expression of human T-cell leukemia virus type 1 (HTLV-1) is regulated by two trans-acting factors encoded by the pX region, p40tax and p27tax.p40tax is a transcriptional activator and p27rex is a post-transcriptional regulator. Using full-length viral DNA, we studied the regulatory effects of rex on HTLV-1 gene expression. p27rex is required for expression of both gag and env proteins, increasing the level of their mRNAs. The effect was dependent on the dose of p27rex expression plasmid. In parallel, increased doses of p27rex suppressed the expression of fully spliced pX mRNA, which encodes the regulatory proteins. These two effects of p27rex operated at the post-transcriptional level and were independent of transcriptional regulation. Lowering the level of pX mRNA down-regulates transcription of the proviral genome. These observations demonstrate that rex is a positive post-transcriptional regulator for gag, pol and env protein expression, and acts at the same time as an indirect negative regulator of viral transcription.

摘要

1型人类T细胞白血病病毒(HTLV-1)的基因表达受pX区域编码的两种反式作用因子p40tax和p27tax调控。p40tax是一种转录激活因子,p27rex是一种转录后调节因子。我们使用全长病毒DNA研究了rex对HTLV-1基因表达的调控作用。p27rex是gag和env蛋白表达所必需的,可增加它们mRNA的水平。这种作用取决于p27rex表达质粒的剂量。同时,增加p27rex的剂量会抑制完全剪接的pX mRNA的表达,该mRNA编码调节蛋白。p27rex的这两种作用在转录后水平发挥,且与转录调控无关。降低pX mRNA的水平会下调前病毒基因组的转录。这些观察结果表明,rex是gag、pol和env蛋白表达的正向转录后调节因子,同时作为病毒转录的间接负向调节因子发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/52c34734c2df/emboj00139-0223-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/3d394cdd7a24/emboj00139-0222-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/68aef48eccc6/emboj00139-0222-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/9ee0dda5bc1f/emboj00139-0223-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/52c34734c2df/emboj00139-0223-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/3d394cdd7a24/emboj00139-0222-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/68aef48eccc6/emboj00139-0222-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/9ee0dda5bc1f/emboj00139-0223-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ef/454349/52c34734c2df/emboj00139-0223-b.jpg

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Current State of Therapeutics for HTLV-1.HTLV-1 的治疗现状。
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