The generality and quantitative extent of alternative splicing have only now begun to be fully appreciated. The first draft of the complete human genome led to the surprisingly low figure of about 32,000 genes. The extensive use of alternative splicing and its consequences in terms of coding capacity could account for this discrepancy and help fill the complexity gap between the genome and the proteome. After a computer-based assessment of the frequency of alternative splicing, this book addresses mechanistic aspects followed by examples of its involvement in important cellular processes. Finally, it raises the possibility of artificial modulation of alternative splicing by antisense nucleotides.
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