ArticleCell death & disease2023
IF1 ablation prevents ATP synthase oligomerization, enhances mitochondrial ATP turnover and promotes an adenosine-mediated pro-inflammatory phenotype.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- ATPIF1, the rheostat in mitochondrial bioenergetics and dysfunction in diseases.Mitochondrion · 2026Review
- Reversal of ATP synthase is a key attribute accompanying cellular differentiation of Trypanosoma brucei insect forms.Communications biology · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.Nature communications · 2026Article
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- Disruption of ATP Synthase Spatiotemporal Organization, CaAging cell · 2026Article
- Levistolide A Alleviates Myocardial Ischemia-Reperfusion Injury Partly by Improving Calcium Homeostasis via the ADORA2B/cAMP/PKA/PLB/SERCA2α Signaling Axis.Current issues in molecular biology · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial function is impaired in long COVID patients.Annals of medicine · 2025Observational
- TheMolecular biology of the cell · 2025Article
- IF1 is a cold-regulated switch of ATP synthase hydrolytic activity to support thermogenesis in brown fat.The EMBO journal · 2024Article
- Variability of Mitochondrial DNA Heteroplasmy: Association with Asymptomatic Carotid Atherosclerosis.Biomedicines · 2024Article
- ThebioRxiv : the preprint server for biology · 2024Article
- Ablation ofiScience · 2024Article
- Review
- The Mitochondrial ATP Synthase/IF1 Axis in Cancer Progression: Targets for Therapeutic Intervention.Cancers · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATPase Inhibitory Factor 1 (IF1) regulates the activity of mitochondrial ATP synthase. The expression of IF1 in differentiated human and mouse cells is highly variable. In intestinal cells, the overexpression of IF1 protects against colon inflammation. Herein, we have developed a conditional IF1-knockout mouse model in intestinal epithelium to investigate the role of IF1 in mitochondrial function and tissue homeostasis. The results show that IF1-ablated mice have increased ATP synthase/hydrolase activities, leading to profound mitochondrial dysfunction and a pro-inflammatory phenotype that impairs the permeability of the intestinal barrier compromising mouse survival upon inflammation. Deletion of IF1 prevents the formation of oligomeric assemblies of ATP synthase and alters cristae structure and the electron transport chain. Moreover, lack of IF1 promotes an intramitochondrial Ca
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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 Socratic graph.