ArticleCell death and differentiation2013
IF1 limits the apoptotic-signalling cascade by preventing mitochondrial remodelling.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 91 citations in OpenAlex.
- OPA1 Requires ATP Synthase Activity and Oligomerization to Mitigate Prion-Induced Mitochondrial Dysfunction, Oxidative Stress, and Neuronal Apoptosis.Molecular neurobiology · 2026Article
- Reversal of ATP synthase is a key attribute accompanying cellular differentiation of Trypanosoma brucei insect forms.Communications biology · 2026Article
- Pathogenic Mechanisms in Cervical Cancer: Energy Metabolism, Hypoxia and Therapy.Life (Basel, Switzerland) · 2026Review
- NMR assignments of the human homodimeric mitochondrial ATP synthase inhibitor IF1.Biomolecular NMR assignments · 2025Article
- NMR assignments of the human homodimeric mitochondrial ATP synthase inhibitor IF1.Research square · 2025Article
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice.Molecular metabolism · 2024Article
- Peptides Targeting the IF1-ATP Synthase Complex Modulate the Permeability Transition Pore in Cancer HeLa Cells.International journal of molecular sciences · 2024Article
- The Pro-Oncogenic Protein IFInternational journal of molecular sciences · 2023Article
- The Mitochondrial ATP Synthase/IF1 Axis in Cancer Progression: Targets for Therapeutic Intervention.Cancers · 2023Review
- IF1 ablation prevents ATP synthase oligomerization, enhances mitochondrial ATP turnover and promotes an adenosine-mediated pro-inflammatory phenotype.Cell death & disease · 2023Article
- 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
- Impact of ATP synthase/coupling factor 6 in hypoxic pulmonary arterial hypertension: An experimental rat model.Turkish journal of medical sciences · 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
- Neuroprotective effects of ATPase inhibitory factor 1 preventing mitochondrial dysfunction in Parkinson's disease.Scientific reports · 2022Article
- Overexpression of GhKTI12 Enhances Seed Yield and Biomass Production in Nicotiana Tabacum.Genes · 2022Article
- The F1Fo-ATPase inhibitor protein IF1 in pathophysiology.Frontiers in physiology · 2022Review
- The ATPase Inhibitory Factor 1 is a Tissue-Specific Physiological Regulator of the Structure and Function of Mitochondrial ATP Synthase: A Closer Look Into Neuronal Function.Frontiers in physiology · 2022Review
- Links between mitochondrial retrograde response and mitophagy in pathogenic cell signalling.Cellular and molecular life sciences : CMLS · 2021Review
- Molecular and Supramolecular Structure of the Mitochondrial Oxidative Phosphorylation System: Implications for Pathology.Life (Basel, Switzerland) · 2021Review
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5 authors at 2 institutions in 1 country.
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Abstract
Mitochondrial structure has a central role both in energy conversion and in the regulation of cell death. We have previously shown that IF1 protects cells from necrotic cell death and supports cristae structure by promoting the oligomerisation of the F1Fo-ATPsynthase. As IF1 is upregulated in a large proportion of human cancers, we have here explored its contribution to the progression of apoptosis and report that an increased expression of IF1, relative to the F1Fo-ATPsynthase, protects cells from apoptotic death. We show that IF1 expression serves as a checkpoint for the release of Cytochrome c (Cyt c) and hence the completion of the apoptotic program. We show that the progression of apoptosis engages an amplification pathway mediated by: (i) Cyt c-dependent release of ER Ca(2+), (ii) Ca(2+)-dependent recruitment of the GTPase Dynamin-related protein 1 (Drp1), (iii) Bax insertion into the outer mitochondrial membrane and (iv) further release of Cyt c. This pathway is accelerated by suppression of IF1 and delayed by its overexpression. IF1 overexpression is associated with the preservation of mitochondrial morphology and ultrastructure, consistent with a central role for IF1 as a determinant of the inner membrane architecture and with the role of mitochondrial ultrastructure in the regulation of Cyt c release. These data suggest that IF1 is an antiapoptotic and potentially tumorigenic factor and may be a valuable predictor of responsiveness to chemotherapy.
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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 OpenQuestion graph.