ArticleRNA biology2022
A novel role for nucleolin in splice site selection.
Article in RNA biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of RNA binding proteins that mediate a quality control mechanism of splicing.bioRxiv : the preprint server for biology · 2025Article
- The Nucleolus and Its Interactions with Viral Proteins Required for Successful Infection.Cells · 2024Review
- COPI coatomer subunit α-COP interacts with the RNA binding protein Nucleolin via a C-terminal dilysine motif.Human molecular genetics · 2023Article
- Identification of G-quadruplex structures in MALAT1 lncRNA that interact with nucleolin and nucleophosmin.Nucleic acids research · 2023Article
- A Quality Control Mechanism of Splice Site Selection Abrogated under Stress and in Cancer.Cancers · 2022Review
- Alternative splicing modulation mediated by G-quadruplex structures in MALAT1 lncRNA.Nucleic acids research · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Latent 5' splice sites, not normally used, are highly abundant in human introns, but are activated under stress and in cancer, generating thousands of nonsense mRNAs. A previously proposed mechanism to suppress latent splicing was shown to be independent of NMD, with a pivotal role for initiator-tRNA independent of protein translation. To further elucidate this mechanism, we searched for nuclear proteins directly bound to initiator-tRNA. Starting with UV-crosslinking, we identified nucleolin (NCL) interacting directly and specifically with initiator-tRNA in the nucleus, but not in the cytoplasm. Next, we show the association of ini-tRNA and NCL with pre-mRNA. We further show that recovery of suppression of latent splicing by initiator-tRNA complementation is NCL dependent. Finally, upon nucleolin knockdown we show activation of latent splicing in hundreds of coding transcripts having important cellular functions. We thus propose nucleolin, a component of the endogenous spliceosome, through its direct binding to initiator-tRNA and its effect on latent splicing, as the first protein of a nuclear quality control mechanism regulating splice site selection to protect cells from latent splicing that can generate defective mRNAs.
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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.