ArticleThe Biochemical journal2015
Transition metals activate TFEB in overexpressing cells.
Article in The Biochemical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
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- Dose-Dependent Reprogramming of Chromatin Accessibility by SOX4 Drives the Transcriptional Response to Iron Overload.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- Role of copper homeostasis and cuproptosis in heart failure pathogenesis: implications for therapeutic strategies.Frontiers in pharmacology · 2024Review
- Recent Progress of Copper-Based Nanomaterials in Tumor-Targeted Photothermal Therapy/Photodynamic Therapy.Pharmaceutics · 2023Review
- Copper metabolism in cell death and autophagy.Autophagy · 2023Review
- Copper metabolism and hepatocellular carcinoma: current insights.Frontiers in oncology · 2023Review
- Evolutionary rate covariation identifies SLC30A9 (ZnT9) as a mitochondrial zinc transporter.The Biochemical journal · 2021Article
- Sulforaphane Activates a lysosome-dependent transcriptional program to mitigate oxidative stress.Autophagy · 2021Article
- Interplay among miR-29 family, mineral metabolism, and gene regulation in Bos indicus muscle.Molecular genetics and genomics : MGG · 2020Article
- Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity.The Biochemical journal · 2019Article
- Current concepts in the neuropathogenesis of mucolipidosis type IV.Journal of neurochemistry · 2019Review
- Proteomic Profiling of Iron-Treated Ovarian Cells Identifies AKT Activation that Modulates the CLEAR Network.Proteomics · 2018Article
- Effects of DHA on Hippocampal Autophagy and Lysosome Function After Traumatic Brain Injury.Molecular neurobiology · 2018Article
- The mucolipin-1 (TRPML1) ion channel, transmembrane-163 (TMEM163) protein, and lysosomal zinc handling.Frontiers in bioscience (Landmark edition) · 2017Review
- Biphasic regulation of lysosomal exocytosis by oxidative stress.Cell calcium · 2016Article
- ROS and intracellular ion channels.Cell calcium · 2016Review
- Transcription factor EB: from master coordinator of lysosomal pathways to candidate therapeutic target in degenerative storage diseases.Annals of the New York Academy of Sciences · 2016Review
- Proteomic analysis of mucopolysaccharidosis I mouse brain with two-dimensional polyacrylamide gel electrophoresis.Molecular genetics and metabolismArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Transition metal toxicity is an important factor in the pathogenesis of numerous human disorders, including neurodegenerative diseases. Lysosomes have emerged as important factors in transition metal toxicity because they handle transition metals via endocytosis, autophagy, absorption from the cytoplasm and exocytosis. Transcription factor EB (TFEB) regulates lysosomal biogenesis and the expression of lysosomal proteins in response to lysosomal and/or metabolic stresses. Since transition metals cause lysosomal dysfunction, we proposed that TFEB may be activated to drive gene expression in response to transition metal exposure and that such activation may influence transition metal toxicity. We found that transition metals copper (Cu) and iron (Fe) activate recombinant TFEB and stimulate the expression of TFEB-dependent genes in TFEB-overexpressing cells. In cells that show robust lysosomal exocytosis, TFEB was cytoprotective at moderate levels of Cu exposure, decreasing oxidative stress as reported by the expression of heme oxygenase-1 (HMOX1) gene. However, at high levels of Cu exposure, particularly in cells with low levels of lysosomal exocytosis, activation of overexpressed TFEB was toxic, increasing oxidative stress and mitochondrial damage. Based on these data, we conclude that TFEB-driven gene network is a component of the cellular response to transition metals. These data suggest limitations and disadvantages of TFEB overexpression as a therapeutic approach.
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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.