ArticleG3 (Bethesda, Md.)2013
Transcriptome Profiling Following Neuronal and Glial Expression of ALS-Linked SOD1 in Drosophila.
Article in G3 (Bethesda, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled 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.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Meta-analysis of Genetic Modifiers Reveals Candidate Dysregulated Pathways in Amyotrophic Lateral Sclerosis.Neuroscience · 2019Pooled it
- Investigating the neuroprotective effects of strawberry extract against diesel soot-induced motor dysfunction in Drosophila: an in-vivo and in-silico study.In silico pharmacology · 2025Article
- RNA-seq analysis reveals changes in mRNA expression during development in Daphnia mitsukuri.BMC genomics · 2024Article
- Origins of nervous tissue susceptibility to ferroptosis.Cell insight · 2023Review
- Downstream Effects of Mutations inInternational journal of molecular sciences · 2022Article
- Review
- Dysregulation of antimicrobial peptide expression distinguishes Alzheimer's disease from normal aging.Aging · 2020Article
- Altered expression of the Cdk5 activator-like protein, Cdk5α, causes neurodegeneration, in part by accelerating the rate of aging.Disease models & mechanisms · 2018Article
- RNA Dysregulation in Amyotrophic Lateral Sclerosis.Frontiers in genetics · 2018Review
- A fruitful endeavor: modeling ALS in the fruit fly.Brain research · 2015Review
- Do the genes of the innate immune response contribute to neuroprotection in Drosophila?Journal of innate immunity · 2015Review
- Investigating cell death mechanisms in amyotrophic lateral sclerosis using transcriptomics.Frontiers in cellular neuroscience · 2013Review
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 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) generally is a late-onset neurodegenerative disease. Mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene account for approximately 20% of familial ALS and 2% of all ALS cases. Although a number of hypotheses have been proposed to explain mutant SOD1 toxicity, the molecular mechanisms of the disease remain unclear. SOD1-linked ALS is thought to function in a non-cell-autonomous manner such that motoneurons are critical for the onset, and glia contribute to progression of the disease. Recently, it has been shown in Drosophila melanogaster that expression of human SOD1 in a subset of neuronal cells causes synaptic transmission defects, modified motor function, and altered sensitivity to compounds that induce oxidative stress. Here we used the Gal4-UAS (Upstream Activation Sequence) system to further characterize flies expressing wild-type Drosophila SOD1 (dSOD1) and the mutant human SOD1
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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.