ReviewMetallomics : integrated biometal science2024
Emerging perspectives of copper-mediated transcriptional regulation in mammalian cell development.
Review in Metallomics : integrated biometal science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed.
- Balancing cellular copper levels via the post-translational regulation of copper transport.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- SF1 regulates the transcription of FDX1 to promote cuproptosis in pediatric sepsis-related acute lung injury by interacting with cJUN.Biology direct · 2026Article
- Sprayable nanozyme hydrogel epigenetically remodels inflammation for diabetic wound regeneration.Nature communications · 2026Article
- Review
- Systematic analysis ofTranslational andrology and urology · 2026Article
- The PBAF chromatin remodeling complex contributes to metal homeostasis through MTF1 regulation.Metallomics : integrated biometal science · 2026Article
- Inhibition of the Sp1/CTR1 axis attenuates cuproptosis and alleviates axonal injury following intracerebral hemorrhage.Frontiers in molecular biosciences · 2026Article
- Cysteine rich intestinal protein 2 links copper homeostasis to translational regulation in primary myoblasts.microPublication biology · 2025Article
- Mitochondrial pathways of copper neurotoxicity: focus on mitochondrial dynamics and mitophagy.Frontiers in molecular neuroscience · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Copper (Cu) is a vital micronutrient necessary for proper development and function of mammalian cells and tissues. Cu mediates the function of redox active enzymes that facilitate metabolic processes and signaling pathways. Cu levels are tightly regulated by a network of Cu-binding transporters, chaperones, and small molecule ligands. Extensive research has focused on the mammalian Cu homeostasis (cuprostasis) network and pathologies, which result from mutations and perturbations. There are roles for Cu-binding proteins as transcription factors (Cu-TFs) and regulators that mediate metal homeostasis through the activation or repression of genes associated with Cu handling. Emerging evidence suggests that Cu and some Cu-TFs may be involved in the regulation of targets related to development-expanding the biological roles of Cu-binding proteins. Cu and Cu-TFs are implicated in embryonic and tissue-specific development alongside the mediation of the cellular response to oxidative stress and hypoxia. Cu-TFs are also involved in the regulation of targets implicated in neurological disorders, providing new biomarkers and therapeutic targets for diseases such as Parkinson's disease, prion disease, and Friedreich's ataxia. This review provides a critical analysis of the current understanding of the role of Cu and cuproproteins in transcriptional regulation.
Indexed as
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What Socratic 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 Socratic graph.