THE HUMAN U1 SNRNP-SPECIFIC U1A PROTEIN INHIBITS POLYADENYLATION OF ITS OWN PREMESSENGER RNA
THE HUMAN U1 SNRNP-SPECIFIC U1A PROTEIN INHIBITS POLYADENYLATION OF ITS OWN PREMESSENGER RNA
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DOI：
10.1016/0092-8674(93)90577-d
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发表时间：
1993-03-26
期刊：
影响因子：
64.5
通讯作者：
GUNDERSON, SI
中科院分区：
文献类型：
--
作者：
BOELENS, WC;JANSEN, EJR;GUNDERSON, SI
编码U1 snRNP特异性U1A蛋白的人、小鼠和非洲爪蟾mRNA在其3'非翻译区（UTR）中含有保守的47 nt区域。体外研究表明，人U1A蛋白结合到保守区域内的两个位点，这两个位点部分类似于先前表征的U1 snRNA上的U1A结合位点。人U1A蛋白在小鼠细胞中的过表达导致内源性小鼠U1A mRNA积累的下调。体外和体内实验证明，过量的U1A蛋白特异性抑制含有来自人U1A mRNA的保守3' UTR的前mRNA的聚腺苷酸化。因此，U1A蛋白通过涉及前体mRNA结合和多聚腺苷酸化抑制的机制调节其自身mRNA的产生。
Human, mouse, and Xenopus mRNAs encoding the U1 snRNP-specific U1A protein contain a conserved 47 nt region in their 3' untranslated regions (UTRs). In vitro studies show that human U1A protein binds to two sites within the conserved region that resemble, in part, the previously characterized U1A-binding site on U1 snRNA. Overexpression of human U1A protein in mouse cells results in down-regulation of endogenous mouse U1A mRNA accumulation. In vitro and in vivo experiments demonstrate that excess U1A protein specifically inhibits polyadenylation of pre-mRNAs that contain the conserved 3' UTR from human U1A mRNA. Thus, U1A protein regulates the production of its own mRNA via a mechanism that involves pre-mRNA binding and inhibition of polyadenylation.