Presence of exon splicing silencers within human immunodeficiency virus type 1 tat exon 2 and tat-rev exon 3: evidence for inhibition mediated by cellular factors.
Presence of exon splicing silencers within human immunodeficiency virus type 1 tat exon 2 and tat-rev exon 3: evidence for inhibition mediated by cellular factors.
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人类免疫缺陷病毒 1 型 tat 外显子 2 和 tat-rev 外显子 3 中存在外显子剪接沉默子：细胞因子介导抑制的证据。
DOI：
10.1128/mcb.15.8.4606
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发表时间：
1995
影响因子：
5.3
通讯作者：
Stoltzfus,CM
中科院分区：
文献类型：
--
作者：
Amendt,BA;Si,ZH;Stoltzfus,CM
Human immunodeficiency virus type 1 (HIV-1) pre-mRNA splicing is regulated in order to maintain pools of unspliced and partially spliced viral RNAs as well as the appropriate levels of multiply spliced mRNAs during virus infection. We have previously described an element intatexon 2 that negatively regulates splicing at the upstreamtat3 splice site 3 (B. A. Amendt, D. Hesslein, L.-J. Chang, and C. M. Stoltzfus, Mol. Cell. Biol. 14:3960-3970, 1994). In this study, we further defined the element to a 20-nucleotide (nt) region which spans the C-terminalvprand N-terminaltatcoding sequences. By analogy with exon splicing enhancer (ESE) elements, we have termed this element an exon splicing silencer (ESS). We show evidence for another negative cis-acting region withintat-revexon 3 of HIV-1 RNA that has sequence motifs in common with a 20-nt ESS element intatexon 2. This sequence is juxtaposed to a purine-rich ESE element to form a bipartite element regulating splicing at the upstreamtat-rev3 splice site. Inhibition of the splicing of substrates containing the ESS element intatexon 2 occurs at an early stage of spliceosome assembly. The inhibition of splicing mediated by the ESS can be specifically abrogated by the addition of competitor RNA. Our results suggest that HIV-1 RNA splicing is regulated by cellular factors that bind to positive and negativeciselements intatexon 2 andtat-revexon 3.
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DOI：
10.1016/s0021-9258(18)53104-5
发表时间：
1993-04
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
J. R. Roesser;K. Liittschwager;S. Leff
通讯作者：
J. R. Roesser;K. Liittschwager;S. Leff
影响因子：
5.3
作者：
C. V. van Oers;G. Adema;H. Zandberg;T. C. Moen;P. D. Baas
通讯作者：
C. V. van Oers;G. Adema;H. Zandberg;T. C. Moen;P. D. Baas
组织特异性 P 元件前 mRNA 剪接的调节需要 RNA 结合蛋白 PSI。
影响因子：
10.5
作者：
Siebel,CW;Kanaar,R;Rio,DC
通讯作者：
Rio,DC
影响因子：
10.5
作者：
KRAINER, AR;CONWAY, GC;KOZAK, D
通讯作者：
KOZAK, D
影响因子：
11.4
作者：
FISCHER, U;MEYER, S;RAUTMANN, G
通讯作者：
RAUTMANN, G