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人类免疫缺陷病毒1型或人类T细胞白血病病毒I型的tat蛋白可在无从头蛋白质合成的情况下激活同源病毒长末端重复序列的转录。

Transcriptional activation of homologous viral long terminal repeats by the human immunodeficiency virus type 1 or the human T-cell leukemia virus type I tat proteins occurs in the absence of de novo protein synthesis.

作者信息

Jeang K T, Shank P R, Kumar A

机构信息

Laboratory of Molecular Virology, National Cancer Institute, Bethesda, MD 20892.

出版信息

Proc Natl Acad Sci U S A. 1988 Nov;85(21):8291-5. doi: 10.1073/pnas.85.21.8291.

DOI:10.1073/pnas.85.21.8291
PMID:2847157
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC282415/
Abstract

The genomes of human retroviruses [human immunodeficiency virus type 1 (HIV-1) and human T-cell leukemia virus (HTLV-I)] encode positive trans-activator proteins, named tat. In the presence of tat, the transcriptional activity of the homologous HIV-1 or HTLV-I long terminal repeat (LTR) promoter is markedly increased. We have constructed mammalian cell lines that contain stably integrated copies of a HIV-1 or a HTLV-I LTR-chloramphenicol acetyltransferase (CAT) gene. When presynthesized HIV-1 or HTLV-I tat proteins were separately introduced into these cells in the presence of cycloheximide, we found a strong increase in the steady-state expression of the homologous viral LTR. Nuclear "run-on" assays verified that this tat-mediated enhancement, occurring in the absence of de novo cellular protein synthesis, was due to increased transcriptional initiation at the LTR promoter. We conclude that one aspect of transcriptional trans-activation of viral LTR by the HIV-1 and HTLV-I tat proteins does not require the production of new cellular proteins.

摘要

人类逆转录病毒[人类免疫缺陷病毒1型（HIV-1）和人类T细胞白血病病毒（HTLV-I）]的基因组编码名为tat的正向反式激活蛋白。在tat存在的情况下，同源HIV-1或HTLV-I长末端重复序列（LTR）启动子的转录活性显著增加。我们构建了含有稳定整合的HIV-1或HTLV-I LTR-氯霉素乙酰转移酶（CAT）基因拷贝的哺乳动物细胞系。当在环己酰亚胺存在的情况下将预先合成的HIV-1或HTLV-I tat蛋白分别引入这些细胞时，我们发现同源病毒LTR的稳态表达大幅增加。细胞核“连续转录”分析证实，这种在不存在新生细胞蛋白质合成的情况下由tat介导的增强作用，是由于LTR启动子处转录起始增加所致。我们得出结论，HIV-1和HTLV-I tat蛋白对病毒LTR进行转录反式激活的一个方面不需要产生新的细胞蛋白质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/6b25103faa52/pnas00300-0473-b.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/9be74f186e12/pnas00300-0471-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/0fee769b8610/pnas00300-0471-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/7b7d381fde98/pnas00300-0471-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/533fd6ca2771/pnas00300-0471-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/9ca4d8de44b0/pnas00300-0472-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/089c89f2eca4/pnas00300-0472-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/494ae0b7b956/pnas00300-0472-c.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/f6c33ada0a1f/pnas00300-0472-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c09/282415/32a267ad4dd5/pnas00300-0472-f.jpg
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