GO:0017077 oxidative phosphorylation uncoupler activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0017077 oxidative phosphorylation uncoupler activity enables proton transfer from the mitochondrial intermembrane space into the mitochondrial matrix, dissipating the proton gradient established by the electron transport chain.
• This proton leak uncouples electron transport from ATP synthesis, converting energy into heat rather than chemical bond energy.
• Classical uncouplers include weakly acidic protonophores such as carbonyl cyanide m-chlorophenylhydrazone (CCCP) and 2,4-dinitrophenol, which shuttle protons across the inner membrane.
• Uncoupling can be mild and protective, as shown for the mitochondria-targeted compound XJB-5-131 in Huntington disease models.
• Environmental toxicants such as naphthenic acids and aetokthonotoxin can act as uncouplers, linking this activity to ecotoxicology and neurological disease.
• Assays for uncoupling activity are used in drug discovery, including screens for inhibitors of mycobacterial oxidative phosphorylation.
Description
GO:0017077 oxidative phosphorylation uncoupler activity is a molecular function that enables the transfer of protons from the mitochondrial intermembrane space into the mitochondrial matrix, dissipating the proton gradient across the mitochondrial inner membrane that is normally established by the electron transport chain during oxidative phosphorylation. This process, often called proton leak, uncouples electron transport and proton generation from ATP synthesis, meaning that the energy derived from substrate oxidation is released as heat instead of being captured in ATP. The term is central to mitochondrial bioenergetics and is distinct from the activity of ATP synthase, which uses the proton gradient to make ATP. Uncoupling proteins (UCPs) and synthetic protonophores both fall under this activity, and their effects range from physiological thermogenesis to pathological mitochondrial dysfunction. Researchers study oxidative phosphorylation uncoupler activity because it directly modulates cellular energy balance, reactive oxygen species production, and cell survival. Pharmacological uncouplers such as CCCP have long been used experimentally to collapse the mitochondrial membrane potential and probe mitochondrial function. More recently, mild uncouplers have been explored as therapeutic agents to reduce oxidative stress in neurodegenerative conditions. In parallel, environmental contaminants with uncoupler activity, such as naphthenic acids and aetokthonotoxin, have been linked to mitochondrial toxicity and disease. Understanding this activity therefore spans basic mitochondrial biology, pharmacology, and toxicology. The activity is also relevant to infectious disease research. A simple assay for inhibitors of mycobacterial oxidative phosphorylation has been developed, highlighting the potential of targeting uncoupling or related processes in Mycobacterium tuberculosis. In addition, modified uncouplers without an acidic group, such as methylated SF 6847, can inhibit oxidative phosphorylation without uncoupling, suggesting the existence of specific uncoupler binding proteins and complex structure-activity relationships. These findings underscore that oxidative phosphorylation uncoupler activity is not a single mechanism but a spectrum of protonophoric and protein-mediated effects.
oxidative phosphorylation uncoupler activity At A Glance
| GO ID | GO:0017077 |
|---|---|
| GO term | oxidative phosphorylation uncoupler activity |
| Ontology | molecular_function |
| Synonym | mitochondrial uncoupling protein activity; uncoupling protein activity |
| Definition | Enables the transfer of protons from mitochondrial intermembrane space into mitochondrial matrix, dissipating the proton gradient across the mitochondrial inner membrane established by the electron transport chain during oxidative phosphorylation (proton leak). Proton leak uncouples the processes of electron transport/proton generation and ATP synthesis. |
| Major function | Proton leak across the mitochondrial inner membrane, uncoupling electron transport from ATP synthesis |
| Cellular location | Mitochondrial inner membrane |
| Representative proteins | Uncoupling proteins (UCP1, UCP2, UCP3), adenine nucleotide translocase (ANT) in some contexts |
| Representative chemicals | CCCP, 2,4-dinitrophenol, SF 6847, XJB-5-131, aetokthonotoxin |
| Related process | Oxidative phosphorylation (GO:0006119), proton transport (GO:0015992) |
What Is GO:0017077?
In our own words, GO:0017077 oxidative phosphorylation uncoupler activity describes the capacity of a protein or chemical to carry protons from the mitochondrial intermembrane space back into the mitochondrial matrix, bypassing ATP synthase. This proton leak dissipates the electrochemical proton gradient that the electron transport chain works to build, so electron transport and ATP synthesis become uncoupled. The activity is a molecular function that can be executed by endogenous uncoupling proteins or by exogenous protonophores, and it results in increased oxygen consumption and heat production without a corresponding increase in ATP synthesis.
Why Is oxidative phosphorylation uncoupler activity Important in Cell Biology?
Oxidative phosphorylation uncoupler activity is important because it sits at the crossroads of energy metabolism, thermogenesis, and cell survival. By dissipating the proton gradient, uncouplers reduce the mitochondrial membrane potential, which can lower reactive oxygen species production and protect cells from oxidative damage, as shown for the mild uncoupler XJB-5-131 in Huntington disease models. At the same time, excessive uncoupling can deplete ATP and trigger metabolic stress, making this activity a double-edged sword in disease. The term is also critical for understanding the mechanisms of environmental toxicants and pharmacological agents that target mitochondria. In drug discovery, assays for uncoupling activity are used to identify inhibitors of oxidative phosphorylation in pathogens such as Mycobacterium tuberculosis. Thus, GO:0017077 is a key molecular function for researchers in mitochondrial biology, neuroscience, toxicology, and infectious disease.
• Regulates cellular energy balance by uncoupling electron transport from ATP synthesis, affecting ATP supply and heat production.
• Mild uncoupling can reduce mitochondrial reactive oxygen species and protect against oxidative stress in neurodegeneration.
• Excessive uncoupling contributes to mitochondrial dysfunction and metabolic collapse in various pathological states.
• Environmental toxicants such as naphthenic acids and aetokthonotoxin act as uncouplers, linking this activity to ecotoxicology and neurological disease.
• Pharmacological uncouplers like CCCP are standard tools to collapse the mitochondrial membrane potential in experiments.
• Uncoupler activity is a potential target for anti-mycobacterial drug discovery.
• Modified uncouplers without an acidic group can inhibit oxidative phosphorylation without uncoupling, revealing complex structure-activity relationships.
• Reserpine has been shown to act as an uncoupler of oxidative phosphorylation, with relevance to its psychoactive properties.
• The activity is relevant to thermogenesis in brown adipose tissue, where UCP1-mediated proton leak generates heat.
• Assays for uncoupling activity are used in high-throughput screening for mitochondrial modulators.
Mechanism, Genes and Research Methods of oxidative phosphorylation uncoupler activity
Protonophoric mechanism of uncoupling
In simple terms: Uncouplers act like proton shuttles that carry hydrogen ions across the mitochondrial membrane, short-circuiting the battery that powers ATP production.
Classical uncouplers of oxidative phosphorylation are weak acids that can transport protons across the mitochondrial inner membrane, bypassing ATP synthase. Terada (1990) reviewed that these compounds dissipate the proton gradient, leading to increased oxygen consumption and heat production without ATP synthesis. The protonophoric mechanism involves protonation of the uncoupler in the intermembrane space, diffusion across the membrane, and release of the proton in the matrix. This cycle collapses the electrochemical proton gradient and uncouples electron transport from ATP synthesis. The activity is not limited to synthetic compounds; endogenous uncoupling proteins (UCPs) can also facilitate proton leak, although their exact mechanism remains debated.
Mild uncoupling and mitochondrial protection
In simple terms: A little bit of uncoupling can be good, because it lowers the membrane potential and reduces harmful reactive oxygen species.
Xun et al. (2022) demonstrated that XJB-5-131, a mitochondria-targeted compound, acts as a mild uncoupler of oxidative phosphorylation. In models of Huntington disease, this mild uncoupling was associated with reduced oxidative stress and improved mitochondrial function. The study suggests that controlled proton leak can be protective by decreasing the mitochondrial membrane potential and thereby limiting electron leak from the respiratory chain. This concept of mild uncoupling has therapeutic implications for neurodegenerative diseases where oxidative damage is a key pathological feature.
Uncoupling by environmental toxicants
In simple terms: Some pollutants can act as uncouplers, poisoning mitochondria by disrupting their energy production.
Kalvani et al. (2024) showed that a model naphthenic acid decouples oxidative phosphorylation through selective inhibition of mitochondrial complex activity. Naphthenic acids are environmental contaminants found in oil sands process-affected water, and their uncoupling activity may contribute to mitochondrial toxicity. In another study, Rebhahn et al. (2025) identified aetokthonotoxin, the causative agent of vacuolar myelinopathy, as an uncoupler of oxidative phosphorylation due to protonophore activity. These findings link GO:0017077 to ecotoxicology and neurological disease, as aetokthonotoxin causes vacuolar myelinopathy in birds and potentially other species.
Uncoupler binding proteins and structure-activity relationships
In simple terms: Some uncouplers may bind to specific proteins, and small changes in their structure can turn them from uncouplers into inhibitors.
Terada et al. (1988) studied a modified weakly acidic uncoupler, methylated SF 6847, which lacks an acidic group and acts as an inhibitor of oxidative phosphorylation without uncoupling activity. This suggested the possible identity of an uncoupler binding protein and highlighted that uncoupling activity depends on specific structural features, such as the presence of an acidic protonatable group. The study also implies that some effects of uncouplers may be mediated by protein binding rather than pure protonophoric action. This complexity is important when interpreting experiments using uncouplers as tools.
Assays for uncoupling activity
In simple terms: Scientists can measure uncoupling by looking at oxygen consumption, membrane potential, or pH changes in mitochondria.
Harden et al. (2024) developed a simple assay for inhibitors of mycobacterial oxidative phosphorylation, which can also detect uncoupling activity. The assay measures oxygen consumption as a proxy for electron transport, and uncoupling typically increases oxygen consumption while decreasing ATP synthesis. Classical uncouplers like CCCP are often used as positive controls in such assays. Iaubasarova et al. (2020) described a mitochondria-targeted derivative of CCCP that acts as an effective mitochondrial recoupler, showing that chemical modification can reverse uncoupling activity. These assays are essential for screening compounds and studying the molecular function in vitro.
Key Genes Involved in GO:0017077 oxidative phosphorylation uncoupler activity
The following genes and proteins are directly or indirectly involved in oxidative phosphorylation uncoupler activity, based on published literature and their roles in mitochondrial proton leak.
| Gene | Major Role | Research Relevance |
|---|---|---|
| UCP1 | Uncoupling protein 1, mediates proton leak in brown adipose tissue for thermogenesis | Target for obesity and metabolic research; model for mild uncoupling |
| UCP2 | Uncoupling protein 2, regulates reactive oxygen species and insulin secretion | Implicated in diabetes and neurodegeneration; studied for mild uncoupling |
| UCP3 | Uncoupling protein 3, expressed in skeletal muscle and heart | Linked to fatty acid metabolism and energy expenditure |
| ANT1 (SLC25A4) | Adenine nucleotide translocase, can exhibit uncoupling activity under certain conditions | Studied in mitochondrial permeability transition and uncoupling |
| ANT2 (SLC25A5) | Adenine nucleotide translocase isoform, involved in mitochondrial energetics | Potential role in uncoupling and cancer metabolism |
| CCCP (chemical) | Classical protonophore uncoupler | Used as a tool to collapse membrane potential |
| 2,4-Dinitrophenol (chemical) | Classical uncoupler | Historical weight-loss agent; toxicology studies |
| SF 6847 (chemical) | Potent uncoupler | Used to study structure-activity relationships |
| XJB-5-131 (chemical) | Mild uncoupler | Therapeutic candidate for Huntington disease |
| Aetokthonotoxin (chemical) | Protonophore uncoupler | Causative agent of vacuolar myelinopathy |
| Naphthenic acid (chemical) | Uncoupler via complex inhibition | Environmental toxicant |
| Reserpine (chemical) | Uncoupler of oxidative phosphorylation | Psychoactive properties linked to uncoupling |
| Mycobacterial oxidative phosphorylation proteins | Targets for inhibitors | Drug discovery for tuberculosis |
| Mitochondrial complex I | Electron transport chain component | Indirectly affected by uncoupling |
| Mitochondrial complex III | Electron transport chain component | Indirectly affected by uncoupling |
| Mitochondrial complex IV | Electron transport chain component | Indirectly affected by uncoupling |
| ATP synthase (complex V) | ATP production | Uncoupling bypasses ATP synthase |
How Is oxidative phosphorylation uncoupler activity Regulated?
Oxidative phosphorylation uncoupler activity is regulated at multiple levels. Endogenous uncoupling proteins (UCPs) are regulated by gene expression, fatty acids, and purine nucleotides, which can inhibit or activate proton leak. For example, UCP1 activity in brown adipose tissue is stimulated by norepinephrine and fatty acids, while ADP and ATP inhibit it. Synthetic uncouplers are regulated by their chemical properties, such as acidity and lipophilicity, which determine their protonophoric ability. Additionally, the activity can be modulated by mitochondrial membrane potential itself, as high potential may favor uncoupling by some proteins. In pathological states, oxidative stress and calcium overload can induce proton leak through the permeability transition pore, contributing to uncoupling. The recoupling effect of mitochondria-targeted CCCP derivatives shows that chemical modification can reverse uncoupling, offering a regulatory handle.
oxidative phosphorylation uncoupler activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| UCP2 | Neurodegeneration, diabetes | UCP2 knockout mice, neuronal cell lines |
| UCP1 | Obesity, thermogenesis | UCP1 knockout mice, brown adipocytes |
| ANT1 | Mitochondrial myopathy, cardiomyopathy | ANT1 knockout mice, patient fibroblasts |
| Aetokthonotoxin target | Vacuolar myelinopathy | Zebrafish or avian models, neuronal cultures |
| Mycobacterial oxidative phosphorylation | Tuberculosis | Mycobacterium tuberculosis cultures, macrophage infection models |
Neurodegeneration and Huntington disease
Mild uncoupling of oxidative phosphorylation has been investigated as a therapeutic strategy for Huntington disease. Xun et al. (2022) showed that XJB-5-131, a mild uncoupler, reduced oxidative stress and improved mitochondrial function in models of Huntington disease. The rationale is that lowering the mitochondrial membrane potential decreases electron leak and reactive oxygen species production, which are implicated in neuronal death. This suggests that pharmacological modulation of GO:0017077 could be beneficial in neurodegenerative conditions, although excessive uncoupling would be detrimental.
Mitochondrial toxicity and environmental disease
Uncoupling activity is a mechanism of toxicity for several environmental contaminants. Aetokthonotoxin, produced by cyanobacteria, causes vacuolar myelinopathy in birds and acts as a protonophore uncoupler. Naphthenic acids, found in oil sands process-affected water, decouple oxidative phosphorylation through selective inhibition of mitochondrial complex activity. These examples link GO:0017077 to neurological and systemic toxicity, highlighting the importance of screening environmental chemicals for uncoupling activity.
Metabolic and psychoactive effects
Reserpine, an antipsychotic and antihypertensive drug, was shown to act as an uncoupler of oxidative phosphorylation, and this activity may contribute to its psychoactive properties. This historical finding illustrates that uncoupling can have pharmacological effects beyond energy metabolism, potentially influencing neurotransmitter release and neuronal function. In addition, classical uncouplers like 2,4-dinitrophenol have been used for weight loss but were abandoned due to toxicity, underscoring the need for controlled uncoupling.
Infectious disease and drug discovery
Mycobacterium tuberculosis relies on oxidative phosphorylation for energy production, and inhibitors of this pathway are being explored as new antibiotics. Harden et al. (2024) developed a simple assay for inhibitors of mycobacterial oxidative phosphorylation, which can detect uncoupling activity. This approach could identify compounds that target mycobacterial energetics, including uncouplers, as potential anti-tuberculosis drugs. Thus, GO:0017077 is relevant to infectious disease research and antimicrobial development.
From oxidative phosphorylation uncoupler activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does gene X regulate proton leak? | Knockout of UCP genes in cell lines, Seahorse assay |
| What is the effect of a point mutation in UCP1 on uncoupling? | Point mutation knock-in in brown adipocytes |
| Can a tagged UCP1 be used to study localization? | Knock-in of fluorescent tag at endogenous locus |
| Does overexpression of UCP2 protect against oxidative stress? | Overexpression in neuronal cell lines, ROS measurement |
| Can CRISPR library screening identify modifiers of uncoupling? | Genome-wide CRISPR knockout library in mitochondria reporter cells |
| Is a candidate drug a mild uncoupler? | Mitochondria-targeted compound testing in isolated mitochondria |
How to Study the oxidative phosphorylation uncoupler activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Seahorse OCR | Oxygen consumption rate | Real-time mitochondrial function and uncoupling |
| TMRM fluorescence | Mitochondrial membrane potential | Detection of uncoupling and recoupling |
| Isolated mitochondria respiration | Oxygen consumption with substrates | Classical uncoupling assays |
| ATP luminescence | ATP levels | Assessment of energy status after uncoupling |
| CRISPR library screening | Gene essentiality or modifier identification | Discovery of uncoupling regulators |
| Proteomics | Protein expression and modifications | Study of UCP regulation |
| RNA-seq | Transcriptional changes | Response to uncouplers |
| Mitochondrial swelling assay | Permeability transition | Differentiate uncoupling from permeability transition |
Seahorse extracellular flux analysis
Seahorse analyzers measure oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) in live cells. Uncoupling activity increases OCR, and this can be quantified by injecting compounds such as CCCP or testing candidate molecules. This method is widely used to assess mitochondrial function and uncoupling in real time.
Mitochondrial membrane potential assays
Fluorescent dyes such as TMRM or JC-1 measure the mitochondrial membrane potential. Uncouplers dissipate the potential, leading to decreased fluorescence. These assays are used to confirm uncoupling activity and to screen for recoupling agents.
Isolated mitochondria respiration
Isolated mitochondria can be used to measure oxygen consumption with substrates and ADP. Uncouplers increase state 4 respiration and decrease respiratory control ratio. This classical approach provides direct evidence of uncoupling.
CRISPR screening for uncoupling modulators
Genome-wide CRISPR knockout or activation screens can identify genes that regulate sensitivity to uncouplers or that modulate proton leak. Cells are treated with sublethal concentrations of uncouplers, and sgRNA enrichment is analyzed by next-generation sequencing. This approach can uncover novel regulators of GO:0017077.
How CRISPR Can Be Used to Study GO:0017077 oxidative phosphorylation uncoupler activity
Knockout
CRISPR knockout of UCP genes (e.g., UCP1, UCP2, UCP3) can be used to study their contribution to proton leak and uncoupling activity. For example, UCP2 knockout cells may show reduced mild uncoupling and increased reactive oxygen species. Knockout of ANT isoforms can also reveal their role in uncoupling. These models are essential to establish causality between a gene and GO:0017077.
Point Mutation
Point mutations in uncoupling proteins can alter proton transport activity. For instance, mutating key acidic residues in UCP1 may abolish uncoupling. CRISPR point mutation knock-in can recreate disease-associated variants or probe structure-function relationships. Such models help distinguish between protonophoric and regulatory functions.
Knock-in
Knock-in of tags (e.g., FLAG, GFP) at endogenous UCP loci allows visualization and immunoprecipitation of uncoupling proteins. This can reveal their localization, interactions, and regulation. Knock-in of reporter genes under the control of UCP promoters can be used to monitor expression in response to uncouplers.
Overexpression
Overexpression of UCPs or other candidate genes can induce mild uncoupling and protect against oxidative stress. For example, UCP2 overexpression in neuronal cells reduces ROS. Overexpression models are useful for gain-of-function studies and for testing therapeutic potential of mild uncoupling.
How EDITGENE Supports oxidative phosphorylation uncoupler activity Research
Researchers studying oxidative phosphorylation uncoupler activity-related genes often need to determine whether a candidate gene is causally involved in proton leak, whether a specific mutation alters uncoupling capacity, or whether overexpression of a gene can mimic mild uncoupling. EDITGENE provides a comprehensive suite of CRISPR services to address these questions with precision and reproducibility.
Contact EDITGENE today to design your custom CRISPR model for oxidative phosphorylation uncoupler activity research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| SLC25A5 Knockout HEK293T Cell Line | EDJ-KQ01 | Human | 292 | Details Get a Quote |
| UCP1 Knockout HEK293 Cell Line | EDJ-KQ1453 | Human | 7350 | Details Get a Quote |
| SLC25A4 Knockout HEK293 Cell Line | EDJ-KQ1627 | Human | 291 | Details Get a Quote |
| UCP2 Knockout HEK293 Cell Line | EDJ-KQ2339 | Human | 7351 | Details Get a Quote |
| UCP3 Knockout HEK293 Cell Line | EDJ-KQ5995 | Human | 7352 | Details Get a Quote |
| SLC25A5 Knockout HeLa Cell Line | EDJ-KQ19991 | Human | 292 | Details Get a Quote |
| SLC25A4 Knockout A-549 Cell Line | EDJ-KQ21334 | Human | 291 | Details Get a Quote |
| SLC25A4 Knockout HCT 116 Cell Line | EDJ-KQ21335 | Human | 291 | Details Get a Quote |
| SLC25A4 Knockout HeLa Cell Line | EDJ-KQ21336 | Human | 291 | Details Get a Quote |
| SLC25A5 Knockout A-549 Cell Line | EDJ-KQ21337 | Human | 292 | Details Get a Quote |
| SLC25A5 Knockout HCT 116 Cell Line | EDJ-KQ21338 | Human | 292 | Details Get a Quote |
| UCP2 Knockout A-549 Cell Line | EDJ-KQ22752 | Human | 7351 | Details Get a Quote |
| UCP2 Knockout HCT 116 Cell Line | EDJ-KQ22753 | Human | 7351 | Details Get a Quote |
| UCP2 Knockout HeLa Cell Line | EDJ-KQ22754 | Human | 7351 | Details Get a Quote |
| UCP3 Knockout A-549 Cell Line | EDJ-KQ29587 | Human | 7352 | Details Get a Quote |
Frequently Asked Questions About oxidative phosphorylation uncoupler activity
What is oxidative phosphorylation uncoupler activity?
It is a molecular function (GO:0017077) that enables protons to leak across the mitochondrial inner membrane, dissipating the proton gradient and uncoupling electron transport from ATP synthesis.
What genes are involved in oxidative phosphorylation uncoupler activity?
Genes include UCP1, UCP2, UCP3, and ANT isoforms, which encode proteins that can mediate proton leak.
How do uncouplers like CCCP work?
CCCP is a weak acid protonophore that carries protons across the mitochondrial inner membrane, collapsing the proton gradient and uncoupling oxidative phosphorylation.
What is the difference between uncoupling and inhibition of oxidative phosphorylation?
Uncoupling increases oxygen consumption while decreasing ATP synthesis, whereas inhibition reduces both electron transport and ATP synthesis.
Can mild uncoupling be therapeutic?
Yes, mild uncouplers like XJB-5-131 have shown protective effects in models of Huntington disease by reducing oxidative stress.
What diseases are linked to uncoupling activity?
Neurodegeneration, mitochondrial toxicity from environmental contaminants, and infectious diseases like tuberculosis are linked to uncoupling.
How is uncoupling activity measured?
Common methods include Seahorse oxygen consumption assays, mitochondrial membrane potential dyes, and isolated mitochondria respiration.
What is the role of UCP1 in uncoupling?
UCP1 mediates proton leak in brown adipose tissue to generate heat, a physiological example of uncoupling.
Are there uncouplers that do not require an acidic group?
Yes, methylated SF 6847 lacks an acidic group and inhibits oxidative phosphorylation without uncoupling, suggesting specific binding interactions.
How can CRISPR help study uncoupling?
CRISPR knockout, point mutation, knock-in, and overexpression models allow researchers to test the causal role of specific genes in uncoupling activity.
Conclusion
GO:0017077 oxidative phosphorylation uncoupler activity is a fundamental molecular function that regulates mitochondrial energy metabolism by dissipating the proton gradient. It is mediated by endogenous uncoupling proteins and exogenous protonophores, with effects ranging from thermogenesis and mild cytoprotection to toxicity and disease. Understanding this activity is crucial for researchers in neurodegeneration, metabolic disorders, toxicology, and infectious disease. CRISPR-based models and functional assays provide powerful tools to dissect the genes and mechanisms underlying uncoupling, and EDITGENE offers comprehensive services to support such studies.
References
- 1. Xun Z et al.. 2022. XJB-5-131 Is a Mild Uncoupler of Oxidative Phosphorylation.. J Huntingtons Dis 11(2):141-151 PMID: 35404288
- 2. Terada H. 1990. Uncouplers of oxidative phosphorylation.. Environ Health Perspect 87:213-8 PMID: 2176586
- 3. Kalvani Z et al.. 2024. A model naphthenic acid decouples oxidative phosphorylation through selective inhibition of mitochondrial complex activity.. Environ Toxicol Pharmacol 107:104386 PMID: 38340910
- 4. Weinbach EC et al.. 1983. Reserpine as an uncoupler of oxidative phosphorylation and the relevance to its psychoactive properties.. Biochem Pharmacol 32(8):1371-7 PMID: 6222736
- 5. Rebhahn VIC et al.. 2025. Aetokthonotoxin, the Causative Agent of Vacuolar Myelinopathy, Uncouples Oxidative Phosphorylation due to Protonophore Activity.. Chem Res Toxicol 38(9):1495-1508 PMID: 40712083
- 6. Harden SA et al.. 2024. A simple assay for inhibitors of mycobacterial oxidative phosphorylation.. J Biol Chem 300(1):105483 PMID: 37992805
- 7. Iaubasarova IR et al.. 2020. The mitochondria-targeted derivative of the classical uncoupler of oxidative phosphorylation carbonyl cyanide m-chlorophenylhydrazone is an effective mitochondrial recoupler.. PLoS One 15(12):e0244499 PMID: 33378414
- 8. Terada H et al.. 1988. Unique action of a modified weakly acidic uncoupler without an acidic group, methylated SF 6847, as an inhibitor of oxidative phosphorylation with no uncoupling activity: possible identity of uncoupler binding protein.. Biochim Biophys Acta 933(1):193-9 PMID: 2894856
