科学网-PTB蛋白(多聚嘧啶串结合蛋白)研究信息分析报告
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銆婄瀛︽椂鎶ャ€?(2010-1-7 A1 瑕侀椈)
 
鏇村闃呰
 
Molecular Cell, , 996-1006, 24 December 2009

doi:10.1016/j.molcel.2009.12.003


Yuanchao XueYu ZhouTongbin WuTuo ZhuXiong JiYoung-Soo KwonChao ZhangGene YeoDouglas L. BlackHui SunXiang-Dong Fu  and Yi Zhang 




Corresponding author

Corresponding author

4 These authors contributed equally to this work


  • Recent transcriptome analysis indicates that > 90% of human genes undergo alternative splicing, underscoring the contribution of differential RNA processing to diverse proteomes in higher eukaryotic cells. The polypyrimidine tract-binding protein PTB is a well-characterized splicing repressor, but PTB knockdown causes both exon inclusion and skipping. Genome-wide mapping of PTB-RNA interactions and construction of a functional RNA map now reveal that dominant PTB binding near a competing constitutive splice site generally induces exon inclusion, whereas prevalent binding close to an alternative site often causes exon skipping. This positional effect was further demonstrated by disrupting or creating a PTB-binding site on minigene constructs and testing their responses to PTB knockdown or overexpression. These findings suggest a mechanism for PTB to modulate splice site competition to produce opposite functional consequences, which may be generally applicable to RNA-binding splicing factors to positively or negatively regulate alternative splicing in mammalian cells.
 
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