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Article

Differential 3′ splice site recognition of SMN1 and SMN2 transcripts by U2AF and U2 snRNP

25 Feb 2009

Abstract excerpt

Spinal Muscular atrophy is a prevalent genetic disease caused by mutation of the SMN1 gene, which encodes the SMN protein involved in assembly of small nuclear ribonucleoprotein (snRNP) complexes. A paralog of the gene, SMN2, cannot provide adequate levels of functional SMN because exon 7 is skipped in a significant fraction of the mature transcripts. A C to T transition located at position 6 of exon 7 is...

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PMID: 19244360
DOI: 10.1261/rna.1273209

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Related research

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Differential 3′ splice site recognition of SMN1 and SMN2 transcripts by U2AF and U2 snRNPPMID 19244360Read ↗

The Regulation and Regulatory Activities of Alternative Splicing of the SMN GeneSemantic proximity Read ↗

Determinants of exon 7 splicing in the spinal muscular atrophy genes, SMN1 and SMN2.Semantic proximity Read ↗

Disruption of an SF2/ASF-dependent exonic splicing enhancer in SMN2 causes spinal muscular atrophy in the absence of SMN1.Semantic proximity Read ↗

U2AF65-Dependent SF3B1 Function in SMN Alternative SplicingSemantic proximity Read ↗

The splicing regulator Sam68 binds to a novel exonic splicing silencer and functions in SMN2 alternative splicing in spinal muscular atrophy.Semantic proximity Read ↗

SMN2 exon 7 splicing is inhibited by binding of hnRNP A1 to a common ESS motif that spans the 3′ splice siteSemantic proximity Read ↗

Modulating role of RNA structure in alternative splicing of a critical exon in the spinal muscular atrophy genesSemantic proximity Read ↗

Bifunctional antisense oligonucleotides provide a trans-acting splicing enhancer that stimulates <i>SMN2</i> gene expression in patient fibroblastsSemantic proximity Read ↗

SMN mutants of spinal muscular atrophy patients are defective in binding to snRNP proteins.Semantic proximity Read ↗

Spinal Muscular Atrophy: SMN2 Pre-mRNA Splicing Corrected by a U7 snRNA Derivative Carrying a Splicing Enhancer SequenceSemantic proximity Read ↗

An intronic element contributes to splicing repression in spinal muscular atrophy.Semantic proximity Read ↗

hnRNP A1 functions with specificity in repression of SMN2 exon 7 splicingSemantic proximity Read ↗

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