ArticleMolecular biology of the cell2003
New insights into the bioenergetics of mitochondrial disorders using intracellular ATP reporters.
Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 73 citations in OpenAlex.
- Phenazine Methosulfate Rewires Mitochondrial Redox Circuits to Restore Membrane Potential and ATP Synthesis Under ETC Blockade in Glioblastoma Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Autoregulation of the real-time kinetics of the human mitochondrial replicative helicase.Nature communications · 2025Article
- Transcriptome analysis of atad3-null zebrafish embryos elucidates possible disease mechanisms.Orphanet journal of rare diseases · 2025Article
- What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025Article
- OXPHOS deficiency induces mitochondrial DNA synthesis through non-canonical AMPK-dependent mRNA compartmentalization.Journal of biosciences · 2022Article
- Nrf2 signaling links ER oxidative protein folding and calcium homeostasis in health and disease.Life science alliance · 2019Article
- Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas.The Journal of clinical investigation · 2019Review
- Rhodamine-based sensor for real-time imaging of mitochondrial ATP in living fibroblasts.Biochimica et biophysica acta. Bioenergetics · 2017Article
- Use of luciferase probes to measure ATP in living cells and animals.Nature protocols · 2017Article
- Exploring cells with targeted biosensors.The Journal of general physiology · 2017Review
- Cooperativity between verapamil and ATP bound to the efflux transporter P-glycoprotein.Biochemical pharmacology · 2016Article
- An EMMPRIN-γ-catenin-Nm23 complex drives ATP production and actomyosin contractility at endothelial junctions.Journal of cell science · 2014Article
- Article
- Screening of effective pharmacological treatments for MELAS syndrome using yeasts, fibroblasts and cybrid models of the disease.British journal of pharmacology · 2012Article
- Mitochondrial DNA mutations provoke dominant inhibition of mitochondrial inner membrane fusion.PloS one · 2012Article
- Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase.Nature cell biology · 2011Article
- Disease variants of the human mitochondrial DNA helicase encoded by C10orf2 differentially alter protein stability, nucleotide hydrolysis, and helicase activity.The Journal of biological chemistry · 2010Article
- Forward operation of adenine nucleotide translocase during F0F1-ATPase reversal: critical role of matrix substrate-level phosphorylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo.PloS one · 2009Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in mitochondrial DNA (mtDNA) cause impairment of ATP synthesis. It was hypothesized that high-energy compounds, such as ATP, are compartmentalized within cells and that different cell functions are sustained by different pools of ATP, some deriving from mitochondrial oxidative phosphorylation (OXPHOS) and others from glycolysis. Therefore, an OXPHOS dysfunction may affect different cell compartments to different extents. To address this issue, we have used recombinant forms of the ATP reporter luciferase localized in different cell compartments- the cytosol, the subplasma membrane region, the mitochondrial matrix, and the nucleus- of cells containing either wild-type or mutant mtDNA. We found that with glycolytic substrates, both wild-type and mutant cells were able to maintain adequate ATP supplies in all compartments. Conversely, with the OXPHOS substrate pyruvate ATP levels collapsed in all cell compartments of mutant cells. In wild-type cells normal levels of ATP were maintained with pyruvate in the cytosol and in the subplasma membrane region, but, surprisingly, they were reduced in the mitochondria and, to a greater extent, in the nucleus. The severe decrease in nuclear ATP content under "OXPHOS-only" conditions implies that depletion of nuclear ATP plays an important, and hitherto unappreciated, role in patients with mitochondrial dysfunction.
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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.