The Clk2 and Clk3 dual-specificity protein kinases regulate the intranuclear distribution of SR proteins and influence pre-mRNA splicing
The Clk2 and Clk3 dual-specificity protein kinases regulate the intranuclear distribution of SR proteins and influence pre-mRNA splicing
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DOI：
10.1006/excr.1998.4083
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发表时间：
1998-06-15
影响因子：
3.7
通讯作者：
Bell, JC
中科院分区：
文献类型：
--
作者：
Duncan, PI;Stojdl, DF;Bell, JC
Clk家族的三个成员（Clk1, 2和3）已被证明经历保守的选择性剪接以产生催化活性（Clk）和非活性（Clk(T)）亚型。原型是小鼠Clk1 (mClk1)，是一种核双特异性激酶，可以与SR蛋白相互作用并引起核再分配。在这项研究中，我们证明了人类Clk2和Clk3 （hClk2和3）也存在于细胞核内，并表现出双特异性激酶活性。截断的同工异构体hClk2(T)和hClk3(T)在核斑点中与SR蛋白共定位。我们还发现具有催化活性的hClk2和hClk3导致SR蛋白的重新分布，并可以调节模型前体mRNA底物在体内的选择性剪接。(C) 1998学术出版社。
The three members of the Clk family of kinases (Clk1, 2, and 3) have been shown to undergo conserved alternative splicing to generate catalytically active (Clk) and inactive (Clk(T)) isoforms. The prototype, murine Clk1 (mClk1), is a nuclear dual-specificity kinase that can interact with, and cause the nuclear redistribution of, SR proteins. In this study, we demonstrate that the human Clk2 and Clk3 (hClk2 and 3) are also found within the nucleus and display dual-specificity kinase activity. The truncated isoforms, hClk2(T) and hClk3(T), colocalize with SR proteins in nuclear speckles. We also show catalytically active hClk2 and hClk3 cause the redistribution of SR proteins and can regulate the alternative splicing of a model precursor mRNA substrate in vivo. (C) 1998 Academic Press.