ReviewFrontiers in physiology2022
The F1Fo-ATPase inhibitor protein IF1 in pathophysiology.
Review in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- ATPIF1, the rheostat in mitochondrial bioenergetics and dysfunction in diseases.Mitochondrion · 2026Review
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- Targeting RuvBL1 disrupts mitochondrial metabolism and structure in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2026Article
- Reversal of ATP synthase is a key attribute accompanying cellular differentiation of Trypanosoma brucei insect forms.Communications biology · 2026Article
- Reversible dissociation of mitochondrial Complex V balances anabolic and energy-generating needs in cancer.iScience · 2026Article
- Immunohistochemical Markers of Mitochondrial Electron Transport Chain Instability in Human Brain Regions: A Study of Aging and Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Charting the circulating proteome in ME/CFS using cross-system profiling to uncover mechanistic insights.Cell reports. Medicine · 2026Article
- Pathogenic Mechanisms in Cervical Cancer: Energy Metabolism, Hypoxia and Therapy.Life (Basel, Switzerland) · 2026Review
- The critical role of Atpif1 in Her2-targeted CAR-T cell therapy for solid tumor via modulation of metabolism and mtDNA-STING signal pathway.Frontiers in immunology · 2026Article
- Peptides Targeting the IF1-ATP Synthase Complex Modulate the Permeability Transition Pore in Cancer HeLa Cells.International journal of molecular sciences · 2024Article
- Small Spleen Peptides (SSPs) Shape Dendritic Cell Differentiation through Modulation of Extracellular ATP Synthesis Profile.Biomolecules · 2024Article
- The anti-inflammatory and tolerogenic potential of small spleen peptides.Frontiers in immunology · 2024Review
- IF1 ablation prevents ATP synthase oligomerization, enhances mitochondrial ATP turnover and promotes an adenosine-mediated pro-inflammatory phenotype.Cell death & disease · 2023Article
- Metabolic landscape in cardiac aging: insights into molecular biology and therapeutic implications.Signal transduction and targeted therapy · 2023Review
- The mitochondrial inhibitor IF1 binds to the ATP synthase OSCP subunit and protects cancer cells from apoptosis.Cell death & disease · 2023Article
- A Mutation in Mouse MT-ATP6 Gene Induces Respiration Defects and Opposed Effects on the Cell Tumorigenic Phenotype.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endogenous inhibitor of ATP synthase is a protein of about 10 kDa, known as IF1 which binds to the catalytic domain of the enzyme during ATP hydrolysis. The main role of IF1 consists of limiting ATP dissipation under condition of severe oxygen deprivation or in the presence of dysfunctions of mitochondrial respiratory complexes, causing a collapse in mitochondrial membrane potential and therefore ATP hydrolysis. New roles of IF1 are emerging in the fields of cancer and neurodegeneration. Its high expression levels in tumor tissues have been associated with different roles favouring tumor formation, progression and evasion. Since discordant mechanisms of action have been proposed for IF1 in tumors, it is of the utmost importance to clarify them in the prospective of defining novel approaches for cancer therapy. Other IF1 functions, including its involvement in mitophagy, may be protective for neurodegenerative and aging-related diseases. In the present review we aim to clarify and discuss the emerging mechanisms in which IF1 is involved, providing a critical view of the discordant findings in the literature.
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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.