ArticleRNA (New York, N.Y.)2012
Biological role of the two overlapping poly(A)-binding protein interacting motifs 2 (PAM2) of eukaryotic releasing factor eRF3 in mRNA decay.
Article in RNA (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- RNA-binding proteins in the mouse lens: Functional classifications, expression profiling, and interaction studies of Carhsp1 with crystallin mRNAs.Developmental biology · 2026Article
- Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.Frontiers in molecular biosciences · 2026Review
- Identification of prognostic biomarkers of sepsis and construction of ceRNA regulatory networks.Scientific reports · 2025Article
- Trypanosoma cruzi eIF4E3- and eIF4E4-containing complexes bind different mRNAs and may sequester inactive mRNAs during nutritional stress.Nucleic acids research · 2025Article
- Concerted action of ataxin-2 and PABPC1-bound mRNA poly(A) tail in the formation of stress granules.Nucleic acids research · 2024Article
- Ataxin-2: a powerful RNA-binding protein.Discover oncology · 2024Review
- Degradation of GSPT1 causes TP53-independent cell death in leukemia while sparing normal hematopoietic stem cells.The Journal of clinical investigation · 2022Article
- Nuclear and cytoplasmic poly(A) binding proteins (PABPs) favor distinct transcripts and isoforms.Nucleic acids research · 2022Article
- LARP1 and LARP4: up close with PABP for mRNA 3' poly(A) protection and stabilization.RNA biology · 2021Review
- Direct evidence that Ataxin-2 is a translational activator mediating cytoplasmic polyadenylation.The Journal of biological chemistry · 2020Article
- Tob2 phosphorylation regulates global mRNA turnover to reshape transcriptome and impact cell proliferation.RNA (New York, N.Y.) · 2020Article
- Article
- Article
- Characterization of the multimeric structure of poly(A)-binding protein on a poly(A) tail.Scientific reports · 2018Article
- Harnessing short poly(A)-binding protein-interacting peptides for the suppression of nonsense-mediated mRNA decay.Scientific reports · 2016Article
- Article
- The interaction of cytoplasmic poly(A)-binding protein with eukaryotic initiation factor 4G suppresses nonsense-mediated mRNA decay.RNA (New York, N.Y.) · 2014Article
- Insights into the evolution and domain structure of Ataxin-2 proteins across eukaryotes.BMC research notes · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic releasing factor GSPT/eRF3 mediates translation termination-coupled mRNA decay via interaction with a cytosolic poly(A)-binding protein (PABPC1). A region of eRF3 containing two overlapping PAM2 (PABPC1-interacting motif 2) motifs is assumed to bind to the PABC domain of PABPC1, on the poly(A) tail of mRNA. PAM2 motifs are also found in the major deadenylases Caf1-Ccr4 and Pan2-Pan3, whose activities are enhanced upon PABPC1 binding to these motifs. Their deadenylase activities are regulated by eRF3, in which two overlapping PAM2 motifs competitively prevent interaction with PABPC1. However, it is unclear how these overlapping motifs recognize PABC and regulate deadenylase activity in a translation termination-coupled manner. We used a dominant-negative approach to demonstrate that the N-terminal PAM2 motif is critical for eRF3 binding to PABPC1 and that both motifs are required for function. Isothermal titration calorimetry (ITC) and NMR analyses revealed that the interaction is in equilibrium between the two PAM2-PABC complexes, where only one of the two overlapping PAM2 motifs is PABC-bound and the other is PABC-unbound and partially accessible to the other PABC. Based on these results, we proposed a biological role for the overlapping PAM2 motifs in the regulation of deadenylase accessibility to PABPC1 at the 3' end of poly(A).
Indexed as
Identifiers
What OpenQuestion holds
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.