ArticleProceedings of the National Academy of Sciences of the United States of America2007
Network of coregulated spliceosome components revealed by zebrafish mutant in recycling factor p110.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- A bioinformatics pipeline for the design of a SART3-targeted cancer vaccine with enhanced immunogenicity.Genomics & informatics · 2026Article
- Article
- Variants in SART3 cause a spliceosomopathy characterised by failure of testis development and neuronal defects.Nature communications · 2023Article
- Zebrafish: A Relevant Genetic Model for Human Primary Immunodeficiency (PID) Disorders?International journal of molecular sciences · 2023Review
- Tip110/SART3-Mediated Regulation of NF-κB Activity by Targeting IκBα Stability Through USP15.Frontiers in oncology · 2022Article
- Serrate-Associated Protein 1, a splicing-related protein, promotes miRNA biogenesis in Arabidopsis.The New phytologist · 2021Article
- The spliceosome factor sart3 regulates hematopoietic stem/progenitor cell development in zebrafish through the p53 pathway.Cell death & disease · 2021Article
- Modelling the developmental spliceosomal craniofacial disorder Burn-McKeown syndrome using induced pluripotent stem cells.PloS one · 2020Article
- Disease modeling of core pre-mRNA splicing factor haploinsufficiency.Human molecular genetics · 2019Article
- Tip110/SART3 regulates IL-8 expression and predicts the clinical outcomes in melanoma.Molecular cancer · 2018Article
- RNA-splicing factor SART3 regulates translesion DNA synthesis.Nucleic acids research · 2018Article
- USP15 regulates dynamic protein-protein interactions of the spliceosome through deubiquitination of PRP31.Nucleic acids research · 2017Article
- Spliceosomal protein eftud2 mutation leads to p53-dependent apoptosis in zebrafish neural progenitors.Nucleic acids research · 2017Article
- Forward Genetic Screens in Zebrafish Identify Pre-mRNA-Processing Pathways Regulating Early T Cell Development.Cell reports · 2016Article
- Fish to Learn: Insights into Blood Development and Blood Disorders from Zebrafish Hematopoiesis.Human gene therapy · 2016Review
- Tip110 Regulates the Cross Talk between p53 and Hypoxia-Inducible Factor 1α under Hypoxia and Promotes Survival of Cancer Cells.Molecular and cellular biology · 2015Article
- Spliceosome assembly in the absence of stable U4/U6 RNA pairing.RNA (New York, N.Y.) · 2015Article
- Tip110 binding to U6 small nuclear RNA and its participation in pre-mRNA splicing.Cell & bioscience · 2015Article
- Knocking Down Snrnp200 Initiates Demorphogenesis of Rod Photoreceptors in Zebrafish.Journal of ophthalmology · 2015Article
- Minor class splicing shapes the zebrafish transcriptome during development.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
Abstract
The spliceosome cycle consists of assembly, catalysis, and recycling phases. Recycling of postspliceosomal U4 and U6 small nuclear ribonucleoproteins (snRNPs) requires p110/SART3, a general splicing factor. In this article, we report that the zebrafish earl grey (egy) mutation maps in the p110 gene and results in a phenotype characterized by thymus hypoplasia, other organ-specific defects, and death by 7 to 8 days postfertilization. U4/U6 snRNPs were disrupted in egy mutant embryos, demonstrating the importance of p110 for U4/U6 snRNP recycling in vivo. Surprisingly, expression profiling of the egy mutant revealed an extensive network of coordinately up-regulated components of the spliceosome cycle, providing a mechanism compensating for the recycling defect. Together, our data demonstrate that a mutation in a general splicing factor can lead to distinct defects in organ development and cause disease.
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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.