ArticlePLoS genetics2016
Prefoldin Promotes Proteasomal Degradation of Cytosolic Proteins with Missense Mutations by Maintaining Substrate Solubility.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 70 citations in OpenAlex.
- Gim3 buffers and potentiates de novo mutations that affect fluconazole susceptibility in yeast.EMBO reports · 2026Article
- Pervasive Divergence in Protein Thermostability is Mediated by Both Structural Changes and Cellular Environments.Molecular biology and evolution · 2025Article
- Hsp70 chaperones, Ssa1 and Ssa2, limit poly(A) binding protein aggregation.Molecular biology of the cell · 2025Article
- Unraveling the Role of Proteinopathies in Parasitic Infections.Biomedicines · 2025Review
- Identification of four mitochondria-related genes in sepsis based on RNA sequencing technology.BMC immunology · 2024Observational
- DIP-MS: ultra-deep interaction proteomics for the deconvolution of protein complexes.Nature methods · 2024Article
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Prefoldin 2 contributes to mitochondrial morphology and function.BMC biology · 2023Article
- Calcineurin stimulation by Cnb1p overproduction mitigates protein aggregation and α-synuclein toxicity in a yeast model of synucleinopathy.Cell communication and signaling : CCS · 2023Article
- The GET pathway is a major bottleneck for maintaining proteostasis in Saccharomyces cerevisiae.Scientific reports · 2023Article
- Artificial Hsp104-mediated systems for re-localizing protein aggregates.Nature communications · 2023Article
- Inactive Proteasomes Routed to Autophagic Turnover Are Confined within the Soluble Fraction of the Cell.Biomolecules · 2022Article
- Review
- Nuclear envelope budding is a response to cellular stress.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- It's not just a phase; ubiquitination in cytosolic protein quality control.Biochemical Society transactions · 2021Review
- Prefoldin Function in Cellular Protein Homeostasis and Human Diseases.Frontiers in cell and developmental biology · 2021Review
- Differential role of cytosolic Hsp70s in longevity assurance and protein quality control.PLoS genetics · 2021Article
- Direct involvement of Hsp70 ATP hydrolysis in Ubr1-dependent quality control.Molecular biology of the cell · 2020Article
- The prefoldin complex stabilizes the von Hippel-Lindau protein against aggregation and degradation.PLoS genetics · 2020Article
- Co-Chaperones in Targeting and Delivery of Misfolded Proteins to the 26S Proteasome.Biomolecules · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Misfolded proteins challenge the ability of cells to maintain protein homeostasis and can accumulate into toxic protein aggregates. As a consequence, cells have adopted a number of protein quality control pathways to prevent protein aggregation, promote protein folding, and target terminally misfolded proteins for degradation. In this study, we employed a thermosensitive allele of the yeast Guk1 guanylate kinase as a model misfolded protein to investigate degradative protein quality control pathways. We performed a flow cytometry based screen to identify factors that promote proteasomal degradation of proteins misfolded as the result of missense mutations. In addition to the E3 ubiquitin ligase Ubr1, we identified the prefoldin chaperone subunit Gim3 as an important quality control factor. Whereas the absence of GIM3 did not impair proteasomal function or the ubiquitination of the model substrate, it led to the accumulation of the poorly soluble model substrate in cellular inclusions that was accompanied by delayed degradation. We found that Gim3 interacted with the Guk1 mutant allele and propose that prefoldin promotes the degradation of the unstable model substrate by maintaining the solubility of the misfolded protein. We also demonstrated that in addition to the Guk1 mutant, prefoldin can stabilize other misfolded cytosolic proteins containing missense mutations.
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.