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与经过条件性加工的大鼠纤连蛋白前体mRNA相互作用的HeLa细胞核因子的特性分析

Characterization of HeLa nuclear factors which interact with a conditionally processed rat fibronectin pre-mRNA.

作者信息

Norton P A, Hynes R O

机构信息

Dept. of Medicine, Roger Williams Hospital, Providence, RI.

出版信息

Biochem Biophys Res Commun. 1993 Aug 31;195(1):215-21. doi: 10.1006/bbrc.1993.2032.

DOI:10.1006/bbrc.1993.2032
PMID:8363603
Abstract

It is demonstrated that several HeLa nuclear proteins interact in a magnesium-dependent fashion with a conditionally processed pre-mRNA derived from an alternatively spliced region of the rat fibronectin gene. HnRNP C proteins crosslink under both permissive and non-permissive conditions (high and low magnesium, respectively), whereas hnRNP I/PTB is observed only under the latter. Thus hnRNP I/PTB represents a potential inhibitor of splicing for this intron. A protein that was observed to crosslink under permissive conditions has been identified as splicing factor U2AF65, which thus represents a candidate positive factor in the splicing of this pre-mRNA. We interpret these results with a working model for the conditional selection of the 3' splice site of alternative exon EIIIB.

摘要

结果表明,几种海拉细胞核蛋白以镁依赖的方式与源自大鼠纤连蛋白基因可变剪接区域的条件性加工前体mRNA相互作用。HnRNP C蛋白在允许和非允许条件下(分别为高镁和低镁)均发生交联,而hnRNP I/PTB仅在后者条件下被观察到。因此,hnRNP I/PTB代表了该内含子剪接的潜在抑制剂。在允许条件下观察到发生交联的一种蛋白质已被鉴定为剪接因子U2AF65,因此它是该前体mRNA剪接中的候选正调控因子。我们用一个关于可变外显子EIIIB的3'剪接位点条件性选择的工作模型来解释这些结果。

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Histone deacetylase activity modulates alternative splicing.组蛋白去乙酰化酶活性调节可变剪接。
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A vertebrate RNA-binding protein Fox-1 regulates tissue-specific splicing via the pentanucleotide GCAUG.一种脊椎动物RNA结合蛋白Fox-1通过五核苷酸GCAUG调控组织特异性剪接。
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Polypyrimidine track-binding protein binding downstream of caspase-2 alternative exon 9 represses its inclusion.聚嘧啶序列结合蛋白结合在半胱天冬酶-2可变外显子9下游,抑制其包含。
J Biol Chem. 2001 Mar 16;276(11):8535-43. doi: 10.1074/jbc.M008924200. Epub 2000 Dec 14.
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The polypyrimidine tract binding protein binds upstream of neural cell-specific c-src exon N1 to repress the splicing of the intron downstream.多嘧啶序列结合蛋白结合在神经细胞特异性c-src基因外显子N1的上游,以抑制下游内含子的剪接。
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