RNAi-mediated PTB depletion leads to enhanced exon definition
RNAi-mediated PTB depletion leads to enhanced exon definition
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DOI：
10.1016/s1097-2765(02)00645-7
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发表时间：
2002-10-01
期刊：
影响因子：
16
通讯作者：
Garcia-Blanco, MA
中科院分区：
文献类型：
--
作者：
Wagner, EJ;Garcia-Blanco, MA
在FGF-R2转录本中互斥使用IIIb或IIIc外显子需要沉默IIIb外显子。这种抑制是由外显子上游和下游的沉默元件介导的。这两种沉默子都结合多嘧啶束结合蛋白（PTB），而PTB结合位点是有效沉默外显子IIIb所必需的。外显子IIIb上游或下游的MS2-PTB融合蛋白的募集导致该外显子的抑制。使用RNAi去除内源性PTB会增加来自minigenes和内源性FGF-R2基因的转录本中外显子IIIb的包含。这些数据表明PTB是体内外显子定义的负调节因子。
Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo.