ArticlePloS one2013
Caspase-8 binding to cardiolipin in giant unilamellar vesicles provides a functional docking platform for bid.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Cardiolipin as a Signaling Hub: Evolutionary Conservation and Programmable Platforms Coupling Mitochondrial Stress to Cell Fate.International journal of molecular sciences · 2026Review
- Review
- Barth Syndrome:Genes · 2025Review
- Multiple entanglements of different cell death pathways, in which caspase-8 and BID interact with cardiolipin*, have been identified.Frontiers in cell and developmental biology · 2025Review
- Cardiolipin's multifaceted role in immune response: a focus on interacting proteins.Frontiers in immunology · 2025Review
- Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024Review
- Actin Polymerization Defects Induce Mitochondrial Dysfunction in Cellular Models of Nemaline Myopathies.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Article
- Article
- Wheel and Deal in the Mitochondrial Inner Membranes: The Tale of CytochromeOxidative medicine and cellular longevity · 2020Review
- Output Regulation and Function Optimization of Mitochondria in Eukaryotes.Frontiers in cell and developmental biology · 2020Review
- Mechanistic Connections between Endoplasmic Reticulum (ER) Redox Control and Mitochondrial Metabolism.Cells · 2019Review
- Article
- Review
- Cutting Edge: Mitochondrial Assembly of the NLRP3 Inflammasome Complex Is Initiated at Priming.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- NME4/nucleoside diphosphate kinase D in cardiolipin signaling and mitophagy.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Initiation and perpetuation of NLRP3 inflammasome activation and assembly.Immunological reviews · 2015Review
- Altered Traffic of Cardiolipin during Apoptosis: Exposure on the Cell Surface as a Trigger for "Antiphospholipid Antibodies".Journal of immunology research · 2015Review
- Disorders of phospholipid metabolism: an emerging class of mitochondrial disease due to defects in nuclear genes.Frontiers in genetics · 2015Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caspase-8 is involved in death receptor-mediated apoptosis in type II cells, the proapoptotic programme of which is triggered by truncated Bid. Indeed, caspase-8 and Bid are the known intermediates of this signalling pathway. Cardiolipin has been shown to provide an anchor and an essential activating platform for caspase-8 at the mitochondrial membrane surface. Destabilisation of this platform alters receptor-mediated apoptosis in diseases such as Barth Syndrome, which is characterised by the presence of immature cardiolipin which does not allow caspase-8 binding. We used a simplified in vitro system that mimics contact sites and/or cardiolipin-enriched microdomains at the outer mitochondrial surface in which the platform consisting of caspase-8, Bid and cardiolipin was reconstituted in giant unilamellar vesicles. We analysed these vesicles by flow cytometry and confirm previous results that demonstrate the requirement for intact mature cardiolipin for caspase-8 activation and Bid binding and cleavage. We also used confocal microscopy to visualise the rupture of the vesicles and their revesiculation at smaller sizes due to alteration of the curvature following caspase-8 and Bid binding. Biophysical approaches, including Laurdan fluorescence and rupture/tension measurements, were used to determine the ability of these three components (cardiolipin, caspase-8 and Bid) to fulfil the minimal requirements for the formation and function of the platform at the mitochondrial membrane. Our results shed light on the active functional role of cardiolipin, bridging the gap between death receptors and mitochondria.
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