ArticleRNA biology2013
U1 snRNP-mediated poly(A) site suppression: beneficial and deleterious for mRNA fate.
Article in RNA biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Study of the RNA splicing kinetics via in vivo 5-EU labeling.RNA (New York, N.Y.) · 2024Article
- A conserved role for the ALS-linked splicing factor SFPQ in repression of pathogenic cryptic last exons.Nature communications · 2021Article
- Pathological mechanism and antisense oligonucleotide-mediated rescue of a non-coding variant suppressing factor 9 RNA biogenesis leading to hemophilia B.PLoS genetics · 2020Article
- Suboptimal RNA-RNA interaction limits U1 snRNP inhibition of canonical mRNA 3' processing.RNA biology · 2019Article
- Exploring the Impact of Cleavage and Polyadenylation Factors on Pre-mRNA Splicing Across Eukaryotes.G3 (Bethesda, Md.) · 2017Article
- Cauliflower mosaic virus Transcriptome Reveals a Complex Alternative Splicing Pattern.PloS one · 2015Article
- A day in the life of the spliceosome.Nature reviews. Molecular cell biology · 2014Review
- Protein phosphatase 2A family members (PP2A and PP6) associate with U1 snRNP and the spliceosome during pre-mRNA splicing.Biochemical and biophysical research communications · 2013Article
- Competition within Introns: Splicing Wins over Polyadenylation via a General Mechanism.Acta naturae · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spliceosomal component U1snRNP commits pre-mRNAs to the splicing pathway. Recently, a nuclear RNA surveillance function has been ascribed to U1, namely the suppression of intronic polyadenylation sites. This surveillance holds regulatory potential as it alters the 3' ends of certain receptor tyrosine kinase mRNAs. However, suppression of 3' end processing by U1 snRNP is also the cause of a severe genetic disorder. We described a 3'UTR point mutation creating a 5'SS leading to U1-mediated suppression of 3' end formation. Thus, the inhibitory function of U1 is both beneficial and deleterious where misled. The exact mechanism of how U1 interferes with 3' end processing remains unclear. According to our data, U1 snRNP already interferes with cleavage or poly(A) site selection instead of directly inhibiting poly(A) polymerase as previously assumed. Here, we present alternative models for U1-mediated poly(A) site suppression and discuss the implications for RNA quality control and disease-related mutations.
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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.