Evidence map›Paper›PMID 24798551›Full record

ArticleJournal of neuroscience research2014

Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila eyes.

Aaron A Burr, Wei-Ling Tsou, Gorica Ristic, Sokol V Todi

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Progressive degeneration in a newResearch square · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. An optimized temporally controlled Gal4 system inFrontiers in neuroscience · 2023
    Article
  11. Cells · 2022
    Article
  12. Article
  13. Roles of α-Synuclein and Disease-Associated Factors inInternational journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Aaron A BurrGraduate Program in Cancer Biology, Wayne State University School of Medicine, Detroit, Michigan; Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan.
Wei-Ling Tsou
Gorica Ristic
Sokol V Todi
Wayne State University · US

Funding

TRAINING PROGRAM IN THE BIOLOGY OF CANCERT32CA009531 · NCI · WAYNE STATE UNIVERSITY · PI Larry H Matherly · 1985 to 2026
$5.3M
Posttranslational Modification of Deubiquitinating Enzymes in NeurodegenerationR00NS064097 · NINDS · WAYNE STATE UNIVERSITY · PI TODI, SOKOL · 2011 to 2013
$724k
NCI NIH HHS T32 CA009531NCI NIH HHS T32-CA009531NINDS NIH HHS R00 NS064097NINDS NIH HHS R00NS064097
6 · The paper itself

Abstract

Age-related neurodegeneration has been studied extensively through the use of model organisms, including the genetically versatile Drosophila melanogaster. Various neurotoxic proteins have been expressed in fly eyes to approximate degeneration occurring in humans, and much has been learned from this heterologous system. Although Drosophila expedites scientific research through rapid generational times and relative inexpensiveness, one factor that can hinder analyses is the examination of milder forms of degeneration caused by some toxic proteins in fly eyes. Whereas several disease proteins cause massive degeneration that is easily observed by examining the external structure of the fly eye, others cause mild degeneration that is difficult to observe externally and requires laborious histological preparation to assess and monitor. Here, we describe a sensitive fluorescence-based method to observe, monitor, and quantify mild Drosophila eye degeneration caused by various proteins, including the polyglutamine disease proteins ataxin-3 (spinocerebellar ataxia type 3) and huntingtin (Huntington's disease), mutant α-synuclein (Parkinson's disease), and Aβ42 (Alzheimer's disease). We show that membrane-targeted green fluorescent protein reports degeneration robustly and quantitatively. This simple yet powerful technique, which is amenable to large-scale screens, can help accelerate studies to understand age-related degeneration and to find factors that suppress it for therapeutic purposes.

Indexed as

alpha-SynucleinAmyloid beta-PeptidesAnimalsAtaxin-3CD8 AntigensDisease Models, AnimalDrosophilaDrosophila melanogasterDrosophila ProteinsGreen Fluorescent ProteinsHumansHuntingtin ProteinMice, TransgenicMicrotubule-Associated ProteinsNerve Tissue ProteinsNuclear Proteinsalpha-SynucleinAmyloid beta-Peptidesamyloid beta-protein (1-42)Ataxin-3ATXN3 protein, humanCD8 AntigensDrosophila ProteinsGAL4 protein, DrosophilaGreen Fluorescent ProteinsHtt protein, DrosophilaHuntingtin ProteinMicrotubule-Associated ProteinsNerve Tissue ProteinsNuclear ProteinsPeptide FragmentsPeptidespolyglutamineRepressor ProteinsTranscription FactorsAlzheimer'sHuntington'sneurodegenerationParkinson'spolyglutaminespinocerebellar ataxia

Identifiers

PMID24798551
PMCPMC4144675
OpenAlexW1594280279

What OpenQuestion holds

Textmetadata
LicenceTDM
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.