Key result
SF2/ASF and hnRNP A1 compete to bind pre-mRNA, with SF2/ASF enhancing U1 snRNP binding to shift splicing downstream, while hnRNP A1 reduces binding to allow affinity-based site selection.
Population
pre-mRNA splicing models using purified components
Design
Preclinical
Authors
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Supports mechanistic studies of alternative splicing in cardiovascular genes; leaves open therapeutic targeting in human disease models.
SF2/ASF and hnRNP A1 compete to bind pre-mRNA, antagonistically regulating alternative 5' splice site selection through their opposite effects on U1 snRNP binding.
Eperon et al. (2000) studied this question. SF2/ASF and hnRNP A1 was evaluated on 5' splice site selection and U1 snRNP binding. SF2/ASF and hnRNP A1 compete to bind pre-mRNA, with SF2/ASF enhancing U1 snRNP binding to shift splicing downstream, while hnRNP A1 reduces binding to allow affinity-based site selection.
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