Abstract
The genetic architecture of schizophrenia is dominated by common variants of small effects, similar to most complex human traits. The majority of the schizophrenia GWAS SNPs reside in non-coding regions where they could act through a variety of regulatory mechanisms, such as alternative splicing to generate schizophrenia-associated isoforms. The brain expresses the most diverse repertoire of isoforms, yet our understanding of brain-specific isoform expression and the mechanisms of their regulation by RNA binding proteins (RBPs) are incomplete.
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