SKIP modifies gene expression by affecting both transcription and splicing
SKIP modifies gene expression by affecting both transcription and splicing
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DOI：
10.1016/j.bbrc.2004.02.077
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发表时间：
2004-04-02
影响因子：
3.1
通讯作者：
Osumi, T
中科院分区：
文献类型：
--
作者：
Nagai, K;Yamaguchi, T;Osumi, T
Skip被描述为转录辅助调节因子和剪接体成分，但这些功能之间的关系尚不清楚。我们发现SKIP从病毒来源的基本启动子激活了报告基因的表达。在一项使用一系列携带不同数量GC盒的报告结构的实验中，Skip对活性较强的启动子显示出更显著的效果。我们还发现，SKIP抑制了荧光素酶报告基因中隐蔽剪接供体位置的异常剪接。此外，SKIP抑制了由人类β-珠蛋白基因中的β-地中海贫血突变产生的额外内含子的剪接。在转染实验中，与含有内含子的报告基因相比，无内含子报告基因的表达水平更高，但被SKIP激活的程度较低。这些结果表明，SKIP通过转录激活和调控Pre-mRNA剪接来影响基因表达。(C)2004 Elsevier Inc.保留所有权利。
SKIP has been described as a transcriptional coregulator as well as a spliceosome component, but the relationship between these functions is not clear. We found that SKIP activated reporter gene expression from the basal promoters of viral origin. SKIP exhibited more prominent effect on the promoters with stronger activities, in an experiment employing a series of reporter constructs carrying different numbers of GC boxes. We also found that SKIP suppressed aberrant splicing at a cryptic splice donor site in the luciferase reporter gene. In addition, SKIP suppressed splicing of an extra intron created by a beta-thalassemia mutation in the human beta-globin gene. In the transfection experiment, an intronless reporter exhibited a higher level of expression, but was less significantly activated by SKIP, than the intron-containing reporter. These results indicate that SKIP affects gene expression by both transcriptional activation and regulation of pre-mRNA splicing. (C) 2004 Elsevier Inc. All rights reserved.