Key result
Recruitment of hnRNP A1 to an exon in vivo efficiently represses splicing, demonstrating that exon splicing silencers can function by recruiting hnRNP A1.
Population
HeLa, SVK14, and 293 cell lines and in vitro transcription models
Comparison
Recruitment of hnRNP A1 to an exon via MS2 coat… vs Empty expression vectors, coat protein alone, or…
Design
Preclinical
Authors
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Supports hnRNP A1-mediated splicing repression in vivo; extends in vitro data but leaves open clinical translation in cardiovascular disease.
The study demonstrates that hnRNP A1 can function to repress splicing and suggests that exon splicing silencers work by recruiting hnRNP A1.
Gatto–Konczak et al. (1999) studied this question. hnRNP A1 recruitment vs. RNA without silencer or empty vector was evaluated on Exon splicing repression. Recruitment of hnRNP A1 to an exon in vivo efficiently represses splicing, demonstrating that exon splicing silencers can function by recruiting hnRNP A1.
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