HIV-1 Tat interacts with cyclin T1 to direct the P-TEFb CTD kinase complex to TAR RNA
HIV-1 Tat interacts with cyclin T1 to direct the P-TEFb CTD kinase complex to TAR RNA
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DOI：
10.1101/sqb.1998.63.371
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发表时间：
1998-01-01
期刊：
影响因子：
--
通讯作者：
Jones, KA
中科院分区：
文献类型：
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作者：
Garber, ME;Wei, P;Jones, KA
图1。HIV-1启动子的转录调控。显示的是HIV-1增强子的最小区域(-85到-300)，它与启动子协同作用，以抵消染色质结构和组蛋白脱乙酰酶复合体的抑制效应。该增强子被建议招募组蛋白乙酰转移酶(HATS)作为转录辅助激活物复合体的一部分。HIV-1Tat在启动后起作用，并通过与TAR RNA结合促进早期伸长。对RNAPII延伸的强烈阻碍是通过在TAR结构形成之前在新生转录中形成的抑制性RNA结构来建立的(Palangat等人。1998年)。RNAPII延长的其他抑制剂可能包括与RNAPII起始复合体相关的CDK抑制剂和CTD磷酸酶，以及HIV-1启动子上的“短转录诱导物”元件(Pessler和Hernandez 1998)。
Figure 1. Transcriptional regulation of the HIV-1 promoter. Shown is the minimal region of the HIV-1 enhancer (–85 to–300) that functions in concert with the promoter to counteract the repressive effects of chromatin structure and histone deacetylase complexes. The enhancer is proposed to recruit histone acetyltransferases (HATs) as part of a transcriptional coactivator complex. HIV-1 Tat acts subsequent to initiation and facilitates an early step in elongation through binding to TAR RNA. A strong block to RNAPII elongation is established by an inhibitory RNA structure that forms in the nascent transcript prior to the formation of the TAR structure (Palangat et al. 1998). Additional inhibitors of RNAPII elongation might include CDK inhibitors and CTD phosphatases associated with the RNAPII initiation complex, as well as the “inducer of short transcripts” element at the HIV-1 promoter (Pessler and Hernandez 1998).