ArticlePloS one2011
Antamanide, a derivative of Amanita phalloides, is a novel inhibitor of the mitochondrial permeability transition pore.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 54 citations in OpenAlex.
- Human Cyclophilins-An Emerging Class of Drug Targets.Medicinal research reviews · 2026Review
- New cyclophilin D inhibitor rescues mitochondrial and cognitive function in Alzheimer's disease.Brain : a journal of neurology · 2024Article
- Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).Molecular medicine reports · 2022Review
- Antamanide Analogs as Potential Inhibitors of Tyrosinase.International journal of molecular sciences · 2022Article
- Sleep/wake calcium dynamics, respiratory function, and ROS production in cardiac mitochondria.Journal of advanced research · 2021Article
- Novel Cyclic Peptides from LethalJournal of fungi (Basel, Switzerland) · 2021Article
- Cyclophilin D, Somehow a Master Regulator of Mitochondrial Function.Biomolecules · 2018Review
- Structural Diversity and Biological Activities of Fungal Cyclic Peptides, Excluding Cyclodipeptides.Molecules (Basel, Switzerland) · 2017Review
- Cyclophilin D ablation is associated with increased end-ischemic mitochondrial hexokinase activity.Scientific reports · 2017Article
- A small-molecule DS44170716 inhibits CaScientific reports · 2017Article
- Expansion and diversification of the MSDIN family of cyclic peptide genes in the poisonous agarics Amanita phalloides and A. bisporigera.BMC genomics · 2016Article
- The entangled ER-mitochondrial axis as a potential therapeutic strategy in neurodegeneration: A tangled duo unchained.Cell calcium · 2016Review
- Identification of a Small Molecule Cyclophilin D Inhibitor for Rescuing Aβ-Mediated Mitochondrial Dysfunction.ACS medicinal chemistry letters · 2016Article
- Mitochondrial permeability transition pore is a potential drug target for neurodegeneration.Biochimica et biophysica acta · 2014Review
- Immunosuppressive peptides and their therapeutic applications.Drug discovery today · 2014Review
- Structure based design, synthesis, pharmacophore modeling, virtual screening, and molecular docking studies for identification of novel cyclophilin D inhibitors.Journal of chemical information and modeling · 2014Article
- Myotonic dystrophy protein kinase (DMPK) prevents ROS-induced cell death by assembling a hexokinase II-Src complex on the mitochondrial surface.Cell death & disease · 2013Article
- Is amyloid binding alcohol dehydrogenase a drug target for treating Alzheimer's disease?Current Alzheimer research · 2013Review
- Inhibition of the Mitochondrial Permeability Transition for Cytoprotection: Direct versus Indirect Mechanisms.Biochemistry research international · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antamanide is a cyclic decapeptide derived from the fungus Amanita phalloides. Here we show that antamanide inhibits the mitochondrial permeability transition pore, a central effector of cell death induction, by targeting the pore regulator cyclophilin D. Indeed, (i) permeability transition pore inhibition by antamanide is not additive with the cyclophilin D-binding drug cyclosporin A, (ii) the inhibitory action of antamanide on the pore requires phosphate, as previously shown for cyclosporin A; (iii) antamanide is ineffective in mitochondria or cells derived from cyclophilin D null animals, and (iv) abolishes CyP-D peptidyl-prolyl cis-trans isomerase activity. Permeability transition pore inhibition by antamanide needs two critical residues in the peptide ring, Phe6 and Phe9, and is additive with ubiquinone 0, which acts on the pore in a cyclophilin D-independent fashion. Antamanide also abrogates mitochondrial depolarization and the ensuing cell death caused by two well-characterized pore inducers, clotrimazole and a hexokinase II N-terminal peptide. Our findings have implications for the comprehension of cyclophilin D activity on the permeability transition pore and for the development of novel pore-targeting drugs exploitable as cell death inhibitors.
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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.