ArticleNucleic acids research2013
SMG5-PNRC2 is functionally dominant compared with SMG5-SMG7 in mammalian nonsense-mediated mRNA decay.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 88 citations in OpenAlex.
- A targetable dependency on nonsense-mediated decay for cellular homeostasis and immune control in small cell lung cancer.Molecular cancer · 2026Article
- Single-cell RNA and DNA methylome profiling reveal liquid helium vitrification enhances porcine parthenogenetically activated blastocyst viability.BMC genomics · 2026Article
- Endonucleolytic cleavage is the primary mechanism of decay elicited byGenome research · 2025Article
- RNA anchoring of Upf1 facilitates recruitment of Dcp2 in the NMD decapping complex.Nucleic acids research · 2025Article
- Human DCP1 is crucial for mRNA decapping and possesses paralog-specific gene regulating functions.eLife · 2024Article
- Transcriptome-wide analysis for glucocorticoid receptor-mediated mRNA decay reveals various classes of target transcripts.Molecules and cells · 2024Article
- Structure of the Nmd4-Upf1 complex supports conservation of the nonsense-mediated mRNA decay pathway between yeast and humans.PLoS biology · 2024Article
- Role of UPF1 in lncRNA-HEIH regulation for hepatocellular carcinoma therapy.Experimental & molecular medicine · 2024Article
- Nonsense-mediated mRNA decay, a simplified view of a complex mechanism.BMB reports · 2023Review
- Keeping development on time: Insights into post-transcriptional mechanisms driving oscillatory gene expression during vertebrate segmentation.Wiley interdisciplinary reviews. RNA · 2023Review
- Vitamin D inhibits osteosarcoma by reprogramming nonsense-mediated RNA decay and SNAI2-mediated epithelial-to-mesenchymal transition.Frontiers in oncology · 2023Article
- Nonsense-mediated RNA decay: an emerging modulator of malignancy.Nature reviews. Cancer · 2022Review
- LC3B is an RNA-binding protein to trigger rapid mRNA degradation during autophagy.Nature communications · 2022Article
- Eukaryotic mRNA Decapping Activation.Frontiers in genetics · 2022Review
- Selective destabilization of polypeptides synthesized from NMD-targeted transcripts.Molecular biology of the cell · 2021Article
- UPF1: From mRNA Surveillance to Protein Quality Control.Biomedicines · 2021Review
- SMG5-SMG7 authorize nonsense-mediated mRNA decay by enabling SMG6 endonucleolytic activity.Nature communications · 2021Article
- Consequences for Pancreatic β-Cell Identity and Function of Unregulated Transcript Processing.Frontiers in endocrinology · 2021Review
- Readthrough of stop codons under limiting ABCE1 concentration involves frameshifting and inhibits nonsense-mediated mRNA decay.Nucleic acids research · 2020Article
- UPF1-Mediated RNA Decay-Danse Macabre in a Cloud.Biomolecules · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, nonsense-mediated mRNA decay (NMD) functions in post-transcriptional gene regulation as well as mRNA surveillance. A key NMD factor, Upf1, becomes hyperphosphorylated by SMG1 kinase during the recognition of NMD substrates. Hyperphosphorylated Upf1 interacts with several factors including SMG5, SMG6, SMG7 and PNRC2 to trigger rapid mRNA degradation. However, the possible cross-talk among these factors and their selective use during NMD remain unknown. Here, we show that PNRC2 is preferentially complexed with SMG5, but not with SMG6 or SMG7, and that downregulation of PNRC2 abolishes the interaction between SMG5 and Dcp1a, a component of the decapping complex. In addition, tethering experiments reveal the function of Upf1, SMG5 and PNRC2 at the same step of NMD and the requirement of SMG6 for Upf1 for efficient mRNA degradation. Intriguingly, microarray results reveal the significant overlap of SMG5-dependent NMD substrates more with PNRC2-dependent NMD substrates than with SMG7-dependent NMD substrates, suggesting the functional dominance of SMG5-PNRC2, rather than SMG5-SMG7, under normal conditions. The results provide evidence that, to some extent, endogenous NMD substrates have their own binding preference for Upf1-interacting adaptors or effectors.
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