Exonic splicing regulatory elements skew synonymous codon usage near intron-exon boundaries in mammals.

Abstract excerpt

In mammals there is a bias in amino acid usage near splice sites that is explained, in large part, by the high density of exonic splicing enhancers (ESEs) in these regions. Is there a similar bias for the relative use of synonymous codons, and can any such bias be predicted by their abundance in ESEs? Prior reports suggested that such trends may exist. From analysis of human exons, we find that 47 of the 59...

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