ReviewFrontiers in physiology2018
A Review of the Inhibition of the Mitochondrial ATP Synthase by IF1
Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 86 citations in OpenAlex.
- ATPIF1, the rheostat in mitochondrial bioenergetics and dysfunction in diseases.Mitochondrion · 2026Review
- Mitochondrial copper stabilizes lipoylated TCA cycle proteins to sustain metabolism and proliferation.bioRxiv : the preprint server for biology · 2026Article
- Life-death trade-offs: HSV-1 ICP27 differentially modulates intrinsic apoptotic signaling in epithelial and neuron-like cells.Frontiers in microbiology · 2026Article
- Mitochondrial Metabolism in T-Cell Exhaustion.International journal of molecular sciences · 2025Review
- Review
- Knockdown of zebrafish tmem242 enhances the production of ROS that signals to increase f9a expression resulting in DIC-like condition.Scientific reports · 2025Article
- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- TheMolecular biology of the cell · 2025Article
- ThebioRxiv : the preprint server for biology · 2024Article
- Small Spleen Peptides (SSPs) Shape Dendritic Cell Differentiation through Modulation of Extracellular ATP Synthesis Profile.Biomolecules · 2024Article
- The Mitochondrial ATP Synthase/IF1 Axis in Cancer Progression: Targets for Therapeutic Intervention.Cancers · 2023Review
- Preservation of mitochondrial membrane potential is necessary for lifespan extension from dietary restriction.GeroScience · 2023Article
- Inhibition of ATP synthase reverse activity restores energy homeostasis in mitochondrial pathologies.The EMBO journal · 2023Article
- Submergence Stress Alters the Expression of Clock Genes and Configures New Zeniths and Expression of Outputs inInternational journal of molecular sciences · 2023Article
- A novel approach to measure complex V ATP hydrolysis in frozen cell lysates and tissue homogenates.Life science alliance · 2023Article
- Article
- Therapeutic Stimulation of Glycolytic ATP Production for Treating ROS-Mediated Cellular Senescence.Metabolites · 2022Article
- Mitochondrial remodeling and ischemic protection by G protein-coupled receptor 35 agonists.Science (New York, N.Y.) · 2022Article
- The Multifaceted ATPase Inhibitory Factor 1 (IF1) in Energy Metabolism Reprogramming and Mitochondrial Dysfunction: A New Player in Age-Associated Disorders?Antioxidants & redox signaling · 2022Review
- New insights into survival strategies to oxygen deprivation in anoxia-tolerant vertebrates.Acta physiologica (Oxford, England) · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ATPase Inhibitory Factor 1 (IF1) is the physiological inhibitor of the mitochondrial ATP synthase. Herein, we summarize the regulation of the expression and activity of IF1 as a main driver of the activity of oxidative phosphorylation (OXPHOS) in mammalian tissues. We emphasize that the expression of IF1, which is a mitochondrial protein with very short half-life, is tissue-specifically expressed and primarily controlled at posttranscriptional levels. Inhibition of the activity of IF1 as inhibitor of the ATP synthase under normal physiological conditions is exerted by phosphorylation of S39 by a cAMP-dependent PKA-like activity of mitochondria in response to different physiological cues. Conditional tissue-specific transgenic mice overexpressing IF1 in colon, or a mutant active version of IF1 (IF1-H49K) in liver or in neurons, revealed the inhibition of the ATP synthase and the reprograming of energy metabolism to an enhanced glycolysis. In the IF1-H49K models, the assembly/activity of complex IV and the superassembly of complex V are also affected. Moreover, the IF1-mediated inhibition of the ATP synthase generates a reactive oxygen species (mtROS) signal that switches on the expression of nuclear genes that facilitate adaptation to a restrained OXPHOS. In contrast to normal mice, metabolically preconditioned animals are partially protected from the action of cytotoxic agents by upgrading the activation of stress kinases and transcription factors involved in resolving metabolic adaptation, the antioxidant response, cell survival, and the immune response of the tissue microenvironment. Altogether, we stress a fundamental physiological function for the ATP synthase and its inhibitor in mitohormesis.
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