ArticleCurrent genetics2012
[NSI+] determinant has a pleiotropic phenotypic manifestation that is modulated by SUP35, SUP45, and VTS1 genes.
Article in Current genetics, 2012. 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
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
8 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Elucidating the regulatory mechanism of Swi1 prion in global transcription and stress responses.Scientific reports · 2020Article
- RNA Sequencing Reveals Specific TranscriptomicSignatures Distinguishing Effects of the [Genes · 2019Article
- Protein Co-Aggregation Related to Amyloids: Methods of Investigation, Diversity, and Classification.International journal of molecular sciences · 2018Review
- Prions and the concept of polyprionic inheritance.Current genetics · 2017Review
- Interaction of Prions Causes Heritable Traits in Saccharomyces cerevisiae.PLoS genetics · 2016Article
- Prions, amyloids, and RNA: Pieces of a puzzle.Prion · 2016Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently discovered the novel non-chromosomal determinant in Saccharomyces cerevisiae [NSI(+)] (nonsense suppression inducer), which causes omnipotent nonsense suppression in strains where the Sup35 N-terminal domain is deleted. [NSI(+)] possesses yeast prion features and does not correspond to previously identified yeast prion determinants. Here, we show that [NSI(+)] enhances nonsense codon read-through and inhibits vegetative growth in S. cerevisiae. Using a large-scale overexpression screen to identify genes that impact the phenotypic effects of [NSI(+)], we found that the SUP35 and SUP45 genes encoding the translation termination factors eRF3 and eRF1, respectively, modulate nonsense suppression in [NSI(+)] strains. The VTS1 gene encodes an NQ-enriched RNA-binding protein that enhances nonsense suppression in [NSI(+)] and [nsi(-)] strains. We demonstrate that VTS1 overexpression, like [NSI(+)] induction, causes translational read-through and growth defects in S. cerevisiae.
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.