ReviewPrion
Are prions part of the dark matter of the cell?
Review in Prion. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 2 citations in OpenAlex.
- Life's code script does not code itself. The machine metaphor for living organisms is outdated.EMBO reports · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The [PSI+] determinant in Saccharomyces cerevisiae is the prion protein corresponding to the eRF3 translation termination factor. Numerous infectious proteins have been described in yeast, in comparison of the unique PrP protein in higher eukaryotes. The presence of the PrP prion is associated with mammalian diseases. Whether fungal prions are beneficial or deleterious are still under discussions. The review focuses on [PSI+]-induced phenotypes and the resulting physiological consequences to shed light on the cellular changes occurring in a [PSI+] cell and its possible role in nature. To date, only two genes directly regulated at the translational level by [PSI+] have been identified. Yet, through all the published works, obtaining a consensus for the described [PSI+] phenotypes appeared a tricky task. They are highly dependent on the prion variant and the genetic background of the strain. The [PSI+] prion might generate diverse modifications not only at the translational, but also at the transcriptional levels, and the phenotypic heterogeneity is the result of these complex combinations of the genotypic expression.
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.