ArticleFly2014
Drosophila models reveal novel insights into mechanisms underlying neurodegeneration.
Article in Fly, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 6 citations in OpenAlex.
- Chromatin binding of Gcn5 in Drosophila is largely mediated by CP190.Nucleic acids research · 2017Article
- Behavioral Senescence and Aging-Related Changes in Motor Neurons and Brain Neuromodulator Levels Are Ameliorated by Lifespan-Extending Reproductive Dormancy inFrontiers in cellular neuroscience · 2017Article
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 2 institutions in 1 country.
Funding
Abstract
The SAGA chromatin modifying complex functions as a transcriptional coactivator for a large number of genes, and SAGA dysfunction has been linked to carcinogenesis and neurodegenerative disease. The protein complex is comprised of approximately 20 subunits, arranged in a modular fashion, and includes 2 enzymatic subunits: the Gcn5 acetyltransferase and the Non-stop deubiquitinase. As we learn more about SAGA, it becomes evident that this complex functions through sophisticated mechanisms that support very precise regulation of gene expression. Here we describe recent findings in which a Drosophila loss-of-function model revealed novel mechanisms for regulation of SAGA-mediated histone H2B deubiquitination. This model also yielded novel and surprising insights into mechanisms that underlie progressive neurodegenerative disease. Lastly, we comment on the utility of Drosophila as a model for neurodegenerative disease through which crucial and conserved mechanisms may be revealed.
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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.