ArticleCell chemical biology2017
Mitochondrial Ferredoxin Determines Vulnerability of Cells to Copper Excess.
Article in Cell chemical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 57 citations in OpenAlex.
- Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- Review
- Copper ionophore elicits calpain-dependent paraptosis coincident with proteotoxic stress.Cell communication and signaling : CCS · 2025Article
- Elesclomol-copper combination synergistically targets mitochondrial metabolism in cancer stem cells to overcome chemoresistance in PDAC.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- An impaired glycolysis induces ATP deficiency and reduced cell respiration in stem cells of patients with autism spectrum disorders.Scientific reports · 2025Article
- Cuproptosis in cancer: biological implications and therapeutic opportunities.Cellular & molecular biology letters · 2024Review
- Superior cuproptotic efficacy of diethyldithiocarbamate-CuFrontiers in pharmacology · 2024Article
- Research progress on cuproptosis in cancer.Frontiers in pharmacology · 2024Review
- Copper-binding proteins genes set predicting the overall survival and immune infiltration in hepatocellular carcinoma by bioinformatic analysis.Biochemistry and biophysics reports · 2023Article
- Full Copper Resistance in Cupriavidus metallidurans Requires the Interplay of Many Resistance Systems.Applied and environmental microbiology · 2023Article
- Functional spectrum and specificity of mitochondrial ferredoxins FDX1 and FDX2.Nature chemical biology · 2023Article
- Mitochondrial copper in human genetic disorders.Trends in endocrinology and metabolism: TEM · 2023Review
- Copper in cancer: from limiting nutrient to therapeutic target.Frontiers in oncology · 2023Review
- Copper homeostasis and cuproptosis in health and disease.Signal transduction and targeted therapy · 2022Review
- ToxPoint: Copper Is the New Showstopper.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Glutathione-dependent redox balance characterizes the distinct metabolic properties of follicular and marginal zone B cells.Nature communications · 2022Article
- A pathogenic role for histone H3 copper reductase activity in a yeast model of Friedreich's ataxia.Science advances · 2021Article
- Transcriptome analysis reveals the encystment-related lncRNA expression profile and coexpressed mRNAs in Pseudourostyla cristata.Scientific reports · 2021Article
- Mitochondrial copper and phosphate transporter specificity was defined early in the evolution of eukaryotes.eLife · 2021Article
- Role of Copper on Mitochondrial Function and Metabolism.Frontiers in molecular biosciences · 2021Review
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
No grant is acknowledged in the PubMed record.
Abstract
The essential micronutrient copper is tightly regulated in organisms, as environmental exposure or homeostasis defects can cause toxicity and neurodegenerative disease. The principal target(s) of copper toxicity have not been pinpointed, but one key effect is impaired supply of iron-sulfur (FeS) clusters to the essential protein Rli1 (ABCE1). Here, to find upstream FeS biosynthesis/delivery protein(s) responsible for this, we compared copper sensitivity of yeast-overexpressing candidate targets. Overexpression of the mitochondrial ferredoxin Yah1 produced copper hyper-resistance.
Indexed as
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.