Evidence map›Paper›PMID 30194090›Full record

ArticleG3 (Bethesda, Md.)2018

Natural Genetic Variation in Yeast Reveals That NEDD4 Is a Conserved Modifier of Mutant Polyglutamine Aggregation.

Theodore W Peters, Christopher S Nelson, Akos A Gerencser, Kathleen J Dumas, Brandon Tavshanjian, Kyu Chul Chang, Gordon J Lithgow, Robert E Hughes

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 47% of its field
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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Integrated regulation of dopaminergic and epigenetic effectors of neuroprotection in Parkinson's disease models.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  2. Ubiquitin-modifying enzymes in Huntington's disease.Frontiers in molecular biosciences · 2023
    Review
  3. Article
  4. Review
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

8 authors at 1 institution in 1 country.

Theodore W PetersBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945 robert.hughes.phd@gmail.com tpeters@alderbio.com.
Christopher S NelsonBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945.
Akos A GerencserBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945.
Kathleen J DumasBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945.ORCID 0000-0003-2694-079X
Brandon TavshanjianBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945.
Kyu Chul ChangBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945.
Gordon J LithgowBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945.
Robert E HughesBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato CA, 94945 robert.hughes.phd@gmail.com tpeters@alderbio.com.
Buck Institute for Research on Aging · US

Funding

Pharmacology of LIfespan ExtensionR01AG029631 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI LITHGOW, GORDON J · 2008 to 2018
$5.4M
Huntingtin interacting proteins as modifiers of Huntington's diseaseR01NS055247 · NINDS · BUCK INSTITUTE FOR RESEARCH ON AGING · PI HUGHES, ROBERT E · 2007 to 2011
$2.1M
Mechanisms of RRAS regulation of huntingtin and turnoverR56NS093392 · NINDS · BUCK INSTITUTE FOR RESEARCH ON AGING · PI HUGHES, ROBERT E · 2015 to 2015
$483k
GENETIC DISSECTION OF NATURAL VARIATION IN CALORIC RESTRICTION-INDUCED CELLULAR LF32AG047024 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI NELSON, CHRISTOPHER S · 2014 to 2016
$164k
NIA NIH HHS F32 AG047024NIA NIH HHS R01 AG029631NINDS NIH HHS R01 NS055247NINDS NIH HHS R56 NS093392
6 · The paper itself

Abstract

A feature common to late onset proteinopathic disorders is an accumulation of toxic protein conformers and aggregates in affected tissues. In the search for potential drug targets, many studies used high-throughput screens to find genes that modify the cytotoxicity of misfolded proteins. A complement to this approach is to focus on strategies that use protein aggregation as a phenotypic readout to identify pathways that control aggregate formation and maintenance. Here we use natural variation between strains of budding yeast to genetically map loci that influence the aggregation of a polyglutamine-containing protein derived from a mutant form of huntingtin, the causative agent in Huntington disease. Linkage analysis of progeny derived from a cross between wild and laboratory yeast strains revealed two polymorphic loci that modify polyglutamine aggregation. One locus contains the gene

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGenetic VariationHEK293 CellsHumansMutationNedd4 Ubiquitin Protein LigasesPeptidesSaccharomyces cerevisiae ProteinsSaccharomycetalesUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingBUL2 protein, S cerevisiaeCaenorhabditis elegans ProteinsNedd4 Ubiquitin Protein LigasesPeptidespolyglutamineRfu1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsUbiquitin-Protein Ligaseswwp-1 protein, C elegansHuntington’s diseasenatural genetic variationpolyglutamineprotein aggregationyeast

Identifiers

PMID30194090
PMCPMC6222566
OpenAlexW2891265331

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.