Abstract
Pre-mRNA splicing is the process in which a ribonucleoprotein complex called the spliceosome removes introns from a primary transcript and ligates its exons together [1]. The spliced exons produce an mRNA containing the mature protein coding sequence. The splicing process is remarkably consistent in its choice of splice sites, and these choices can be regulated to allow different mRNA sequences to arise from the same pre-mRNA transcript, in a process called alternative splicing. In this way, genes often yield multiple mRNAs and encoded proteins to increase diversity of eukaryotic proteomes. Alternative splicing patterns often show developmental and tissue-specific expression. Misregulation of splicing is seen in human disease and can be a direct cause of pathology [2]. Splicing regulatory mechanisms thus present a promising target for therapeutic intervention.
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