ArticleRNA biology2019
Suboptimal RNA-RNA interaction limits U1 snRNP inhibition of canonical mRNA 3' processing.
Article in RNA biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 15 citations in OpenAlex.
- Coupling of alternative splicing and alternative polyadenylation.Acta biochimica et biophysica Sinica · 2024Review
- U4 snRNP inhibits premature cleavage and polyadenylation of pre-mRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The U1 antisense morpholino oligonucleotide (AMO) disrupts U1 snRNP structure to promote intronic PCPA modification of pre-mRNAs.The Journal of biological chemistry · 2023Article
- U1 snRNP proteins promote proximal alternative polyadenylation sites by directly interacting with 3' end processing core factors.Journal of molecular cell biology · 2022Article
- CFIm25 regulates human stem cell function independently of its role in mRNA alternative polyadenylation.RNA biology · 2022Article
- U1 snRNP telescripting: molecular mechanisms and beyond.RNA biology · 2021Review
- Pathological mechanism and antisense oligonucleotide-mediated rescue of a non-coding variant suppressing factor 9 RNA biogenesis leading to hemophilia B.PLoS genetics · 2020Article
- Discovery of alternative polyadenylation dynamics from single cell types.Computational and structural biotechnology journal · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is increasingly appreciated that U1 snRNP transcriptomically suppresses the usage of intronic polyadenylation site (PAS) of mRNAs, an outstanding question is why frequently used PASs are not suppressed. Here we found that U1 snRNP could be transiently associated with sequences upstream of actionable PASs in human cells, and RNA-RNA interaction might contribute to the association. By focusing on individual PAS, we showed that the stable assembly of U1 snRNP near PAS might be generally required for U1 inhibition of mRNA 3' processing. Therefore, actionable PASs that often lack optimal U1 snRNP docking site nearby is free from U1 inhibitory effect. Consistently, natural 5' splicing site (5'-SS) is moderately enriched ~250 nt upstream of intronic PASs whose usage is sensitive to functional knockdown of U1 snRNA. Collectively, our results provided an insight into how U1 snRNP selectively inhibits the usage of PASs in a cellular context, and supported a prevailing model that U1 snRNP scans pre-mRNA through RNA-RNA interaction to find a stable interaction site to exercise its function in pre-mRNA processing, including repressing the usage of cryptic PASs.
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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.