ArticleRNA (New York, N.Y.)2009
Differential 3' splice site recognition of SMN1 and SMN2 transcripts by U2AF and U2 snRNP.
Article in RNA (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Evaluation of SMN protein, transcript, and copy number in the biomarkers for spinal muscular atrophy (BforSMA) clinical study.PloS one · 2012Trial
- Nusinersen: the antisense oligonucleotide at the forefront of spinal muscular atrophy treatment.RNA biology · 2026Review
- Deployment of non-canonical splicing in tunicate genomes is mediated by divergent U2AF function and changing m6A modification in U1 and U6 snRNA.Nucleic acids research · 2026Article
- Spinal Muscular Atrophy: The Past, Present, and Future of Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- Exon-independent recruitment of SRSF1 is mediated by U1 snRNP stem-loop 3.The EMBO journal · 2022Article
- hnRNP A/B Proteins: An Encyclopedic Assessment of Their Roles in Homeostasis and Disease.Biology · 2021Review
- A high-throughput genome-wide RNAi screen identifies modifiers of survival motor neuron protein.Cell reports · 2021Article
- Skipping of an exon with a nonsense mutation in the DMD gene is induced by the conversion of a splicing enhancer to a splicing silencer.Human genetics · 2019Article
- Binding to SMN2 pre-mRNA-protein complex elicits specificity for small molecule splicing modifiers.Nature communications · 2017Article
- Stoichiometries of U2AF35, U2AF65 and U2 snRNP reveal new early spliceosome assembly pathways.Nucleic acids research · 2017Article
- Splicing inhibition of U2AF65 leads to alternative exon skipping.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Genomic functions of U2AF in constitutive and regulated splicing.RNA biology · 2015Article
- A targeted oligonucleotide enhancer of SMN2 exon 7 splicing forms competing quadruplex and protein complexes in functional conditions.Cell reports · 2014Article
- Article
- Ets1 and heat shock factor 1 regulate transcription of the Transformer 2β gene in human colon cancer cells.Journal of gastroenterology · 2013Article
- Antisense oligonucleotides for the treatment of spinal muscular atrophy.Human gene therapy · 2013Review
- Intron retention in the alternatively spliced region of RON results from weak 3' splice site recognition.PloS one · 2013Article
- Nuclear matrix factor hnRNP U/SAF-A exerts a global control of alternative splicing by regulating U2 snRNP maturation.Molecular cell · 2012Article
- A role for SMN exon 7 splicing in the selective vulnerability of motor neurons in spinal muscular atrophy.Molecular and cellular biology · 2012Article
- Design principles for bifunctional targeted oligonucleotide enhancers of splicing.Nucleic acids research · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
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 critical for the difference in exon skipping between SMN1 and SMN2. Here we report that this nucleotide difference results in increased ultraviolet light-mediated crosslinking of the splicing factor U2AF(65) with the 3' splice site of SMN1 intron 6 in HeLa nuclear extract. U2 snRNP association, analyzed by native gel electrophoresis, is also more efficient on SMN1 than on SMN2, particularly under conditions of competition, suggesting more effective use of limiting factors. Two trans-acting factors implicated in SMN regulation, SF2/ASF and hnRNP A1, promote and repress, respectively, U2 snRNP recruitment to both RNAs. Interestingly, depending on the transcript and the regulatory factor, the effects on U2 binding not always correlate with changes in U2AF(65) crosslinking. Furthermore, blocking recognition of a Tra2-beta1-dependent splicing enhancer located in exon 7 inhibits U2 snRNP recruitment without affecting U2AF(65) crosslinking. Collectively, the results suggest that both U2AF binding and other steps of U2 snRNP recruitment can be control points in SMN splicing regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.