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Counterregulation of chromatin deacetylation and histone deacetylase occupancy at the integrated promoter of human immunodeficiency virus type 1 (HIV-1) by the HIV-1 repressor YY1 and HIV-1 activator Tat.人类免疫缺陷病毒1型(HIV-1)的阻遏蛋白YY1和激活蛋白Tat对HIV-1整合启动子处染色质去乙酰化和组蛋白去乙酰化酶占据的反向调节。
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Biochemistry. 1999 Aug 17;38(33):10801-7. doi: 10.1021/bi9912847.
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通过吡咯-咪唑聚酰胺对1型人类免疫缺陷病毒长末端重复序列进行靶向去抑制。

Targeted derepression of the human immunodeficiency virus type 1 long terminal repeat by pyrrole-imidazole polyamides.

作者信息

Coull Jason J, He Guocheng, Melander Christian, Rucker Victor C, Dervan Peter B, Margolis David M

机构信息

Division of Infectious Diseases, Department of Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390, USA.

出版信息

J Virol. 2002 Dec;76(23):12349-54. doi: 10.1128/jvi.76.23.12349-12354.2002.

DOI:10.1128/jvi.76.23.12349-12354.2002
PMID:12414976
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC136904/
Abstract

The host factor LSF represses the human immunodeficiency virus type 1 long terminal repeat (LTR) by mediating recruitment of histone deacetylase. We show that pyrrole-imidazole polyamides targeted to the LTR can specifically block LSF binding both in vitro and within cells via direct access to chromatin, resulting in increased LTR expression.

摘要

宿主因子LSF通过介导组蛋白去乙酰化酶的募集来抑制1型人类免疫缺陷病毒(HIV-1)的长末端重复序列(LTR)。我们发现,靶向LTR的吡咯-咪唑聚酰胺能够通过直接作用于染色质,在体外和细胞内特异性地阻断LSF的结合,从而导致LTR表达增加。