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An exon skipping-associated nonsense mutation in the dystrophin gene uncovers a complex interplay between multiple antagonistic splicing elements
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An apparent pseudo-exon acts both as an alternative exon that leads to nonsense-mediated decay and as a zero-length exon
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Evolutionarily conserved and diverged alternative splicing events show different expression and functional profiles
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A negative element in SMN2 exon 7 inhibits splicing in spinal muscular atrophy
T Kashima et al.
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Mutations in tau gene exon 10 associated with FTDP-17 alter the activity of an exonic splicing enhancer to interact with Tra2β
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hnRNP-G promotes exon 7 inclusion of survival motor neuron (SMN) via direct interaction with Htra2-β1
Y Hofmann et al.
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