ArticleThe EMBO journal2002
Protein 61K, encoded by a gene (PRPF31) linked to autosomal dominant retinitis pigmentosa, is required for U4/U6*U5 tri-snRNP formation and pre-mRNA splicing.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 174 citations in OpenAlex.
- A novel PRPF31 mutation in a large Chinese family with autosomal dominant retinitis pigmentosa and macular degeneration.PloS one · 2013Trial
- Neurodegenerative spliceosomopathies.Frontiers in cell and developmental biology · 2026Review
- Alternative Splicing Dysregulation in Retinitis Pigmentosa: Pathogenic Mechanisms and Therapeutic Opportunities.Biomolecules · 2025Review
- A guide to the biogenesis and functions of endogenous small non-coding RNAs in animals.Nature reviews. Molecular cell biology · 2025Review
- Retinitis pigmentosa-linked mutations impair the snRNA unwinding activity of SNRNP200 and reduce pre-mRNA binding of PRPF8.Cellular and molecular life sciences : CMLS · 2025Article
- A Precision Therapy Approach for Retinitis Pigmentosa 11 Using Splice-Switching Antisense Oligonucleotides to Restore the Open Reading Frame of PRPF31.International journal of molecular sciences · 2024Article
- The splicing factor Prpf31 is required for hematopoietic stem and progenitor cell expansion during zebrafish embryogenesis.The Journal of biological chemistry · 2024Article
- PRPF31-retinitis pigmentosa: Challenges and opportunities for clinical translation.Vision research · 2023Review
- Retinal organoids provide unique insights into molecular signatures of inherited retinal disease throughout retinogenesis.Journal of anatomy · 2023Review
- Review
- Determinants of Disease Penetrance inGenes · 2021Article
- TSSC4 is a component of U5 snRNP that promotes tri-snRNP formation.Nature communications · 2021Article
- SANS (USH1G) regulates pre-mRNA splicing by mediating the intra-nuclear transfer of tri-snRNP complexes.Nucleic acids research · 2021Article
- Prpf31 is essential for the survival and differentiation of retinal progenitor cells by modulating alternative splicing.Nucleic acids research · 2021Article
- Pre-mRNA Processing Factors and Retinitis Pigmentosa: RNA Splicing and Beyond.Frontiers in cell and developmental biology · 2021Review
- Mutation spectrum of PRPF31, genotype-phenotype correlation in retinitis pigmentosa, and opportunities for therapy.Experimental eye research · 2020Review
- Deubiquitinase USP47-stabilized splicing factor IK regulates the splicing ofCell death discovery · 2020Article
- Retinal pigment epithelium degeneration caused by aggregation of PRPF31 and the role of HSP70 family of proteins.Molecular medicine (Cambridge, Mass.) · 2019Article
- Smu1 and RED are required for activation of spliceosomal B complexes assembled on short introns.Nature communications · 2019Article
- A bioinformatic analysis identifies circadian expression of splicing factors and time-dependent alternative splicing events in the HD-MY-Z cell line.Scientific reports · 2019Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In each round of nuclear pre-mRNA splicing, the U4/U6*U5 tri-snRNP must be assembled from U4/U6 and U5 snRNPs, a reaction that is at present poorly understood. We have characterized a 61 kDa protein (61K) found in human U4/U6*U5 tri-snRNPs, which is homologous to yeast Prp31p, and show that it is required for this step. Immunodepletion of protein 61K from HeLa nuclear extracts inhibits tri-snRNP formation and subsequent spliceosome assembly and pre-mRNA splicing. Significantly, complementation with recombinant 61K protein restores each of these steps. Protein 61K is operationally defined as U4/U6 snRNP-specific as it remains bound to this particle at salt concentrations where the tri-snRNP dissociates. However, as shown by two-hybrid analysis and biochemical assays, protein 61K also interacts specifically with the U5 snRNP-associated 102K protein, indicating that it physically tethers U4/U6 to the U5 snRNP to yield the tri-snRNP. Interestingly, protein 61K is encoded by a gene (PRPF31) that has been shown to be linked to autosomal dominant retinitis pigmentosa. Thus, our studies suggest that disruptions in tri-snRNP formation and function resulting from mutations in the 61K protein may contribute to the manifestation of this disease.
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