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通过拮抗剪接因子的过表达在体内调节可变剪接

Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors.

作者信息

Cáceres J F, Stamm S, Helfman D M, Krainer A R

机构信息

Cold Spring Harbor Laboratory, NY 11724.

出版信息

Science. 1994 Sep 16;265(5179):1706-9. doi: 10.1126/science.8085156.

DOI:10.1126/science.8085156
PMID:8085156
Abstract

The opposing effects of SF2/ASF and heterogeneous nuclear ribonucleoprotein (hnRNP) A1 influence alternative splicing in vitro. SF2/ASF or hnRNP A1 complementary DNAs were transiently overexpressed in HeLa cells, and the effect on alternative splicing of several cotransfected reporter genes was measured. Increased expression of SF2/ASF activated proximal 5' splice sites, promoted inclusion of a neuron-specific exon, and prevented abnormal exon skipping. Increased expression of hnRNP A1 activated distal 5' splice sites. Therefore, variations in the intracellular levels of antagonistic splicing factors influence different modes of alternative splicing in vivo and may be a natural mechanism for tissue-specific or developmental regulation of gene expression.

摘要

SF2/ASF和不均一核核糖核蛋白(hnRNP)A1的相反作用在体外影响可变剪接。将SF2/ASF或hnRNP A1互补DNA在HeLa细胞中瞬时过表达,并检测其对几种共转染报告基因可变剪接的影响。SF2/ASF表达增加激活近端5'剪接位点,促进神经元特异性外显子的包含,并防止异常外显子跳跃。hnRNP A1表达增加激活远端5'剪接位点。因此,拮抗剪接因子细胞内水平的变化在体内影响可变剪接的不同模式,并且可能是基因表达的组织特异性或发育调控的天然机制。

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Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors.通过拮抗剪接因子的过表达在体内调节可变剪接
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