Evidence map›Paper›PMID 22052350›Full record

ReviewPrion

Modeling Huntington disease in yeast: perspectives and future directions.

Robert P Mason, Flaviano Giorgini

Abstract readReview
In one paragraph

Review in Prion. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed.

  1. Yeast as a Model for Human Disease.International journal of molecular sciences · 2026
    Review
  2. Vitamin B3 Biotech · 2023
    Article
  3. Validation of the Pathogenic Effect ofInternational journal of molecular sciences · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. NADFrontiers in molecular biosciences · 2021
    Review
  8. Article
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  16. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Robert P MasonDepartment of Genetics, University of Leicester, Leicester, UK.
Flaviano Giorgini

Funding

Medical Research Council G0700090
6 · The paper itself

Abstract

Yeast have been extensively used to model aspects of protein folding diseases, yielding novel mechanistic insights and identifying promising candidate therapeutic targets. In particular, the neurodegenerative disorder Huntington disease (HD), which is caused by the abnormal expansion of a polyglutamine tract in the huntingtin (htt) protein, has been widely studied in yeast. This work has led to the identification of several promising therapeutic targets and compounds that have been validated in mammalian cells, Drosophila and rodent models of HD. Here we discuss the development of yeast models of mutant htt toxicity and misfolding, as well as the mechanistic insights gleaned from this simple model. The role of yeast prions in the toxicity/misfolding of mutant htt is also highlighted. Furthermore, we provide an overview of the application of HD yeast models in both genetic and chemical screens, and the fruitful results obtained from these approaches. Finally, we discuss the future of yeast in neurodegenerative research, in the context of HD and other diseases.

Indexed as

AnimalsHumansHuntington DiseasePeptidesPrionsProtein FoldingRecombinant Fusion ProteinsSaccharomyces cerevisiaePeptidespolyglutaminePrionsRecombinant Fusion Proteins

Identifiers

PMID22052350
PMCPMC4012407

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.