ArticlePloS one2014
U2 snRNP is required for expression of the 3' end of genes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Alternative polyadenylation regulation in cardiac development and cardiovascular disease.Cardiovascular research · 2023Review
- Splicing modulators elicit global translational repression by condensate-prone proteins translated from introns.Cell chemical biology · 2022Article
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- Splicing modulators: on the way from nature to clinic.The Journal of antibiotics · 2021Review
- Titration of SF3B1 Activity Reveals Distinct Effects on the Transcriptome and Cell Physiology.International journal of molecular sciences · 2020Article
- Rbm38 Reduces the Transcription Elongation Defect of theInternational journal of molecular sciences · 2020Article
- Molecular basis of differential 3' splice site sensitivity to anti-tumor drugs targeting U2 snRNP.Nature communications · 2017Article
- Posttranscriptional mechanisms controlling diurnal gene expression cycles by body temperature rhythms.RNA biology · 2017Review
- Targeting cleavage and polyadenylation specific factor 1 via shRNA inhibits cell proliferation in human ovarian cancer.Journal of biosciences · 2017Article
- Global analysis of pre-mRNA subcellular localization following splicing inhibition by spliceostatin A.RNA (New York, N.Y.) · 2017Article
- Temperature regulates splicing efficiency of the cold-inducible RNA-binding protein gene Cirbp.Genes & development · 2016Article
- A Conserved Nuclear Cyclophilin Is Required for Both RNA Polymerase II Elongation and Co-transcriptional Splicing in Caenorhabditis elegans.PLoS genetics · 2016Article
- Article
- Splicing inhibition decreases phosphorylation level of Ser2 in Pol II CTD.Nucleic acids research · 2015Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pre-mRNA in eukaryotes is subjected to mRNA processing, which includes capping, polyadenylation, and splicing. Transcription and mRNA processing are coupled, and this coupling stimulates mRNA processing; however, the effects of mRNA processing on transcription are not fully understood. In this study, we found that inhibition of U2 snRNP by a splicing inhibitor, spliceostatin A (SSA), or by an antisense oligonucleotide to U2 snRNA, caused gene-specific 3'-end down-regulation. Removal of SSA from the culture media restored expression of the 3' ends of genes, suggesting that U2 snRNP is required for expression of the 3' end of genes. Finally, we found that SSA treatment caused accumulation of Pol II near the 5' end of 3'-end down regulated genes, such as CDK6, SMEK2 and EGFR, indicating that SSA treatment led to transcription elongation arrest on these genes. These findings suggest that U2 snRNP is important for production of full length mRNA probably through regulation of transcription elongation, and that a novel checkpoint mechanism prevents pre-mRNA from accumulating as a result of splicing deficiencies, and thereby prevents production of aberrant proteins that might be translated from pre-mRNAs through the arrest of transcription elongation.
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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.