ArticleCell death and differentiation2016
Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 54 citations in OpenAlex.
- MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.Nature structural & molecular biology · 2026Article
- Review
- Neuronal FGF13 Inhibits Mitochondria-Derived Damage Signals to Prevent Neuroinflammation and Neurodegeneration in a Mouse Model of Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ARMC1 partitions between distinct complexes and assembles MIRO with MTFR to control mitochondrial distribution.Science advances · 2025Article
- Bid Protein: A Participant in the Apoptotic Network with Roles in Viral Infections.International journal of molecular sciences · 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
- MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction.Drug design, development and therapy · 2024Review
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- Apoptosis Regulation in Osteoarthritis and the Influence of Lipid Interactions.International journal of molecular sciences · 2023Review
- A BAK subdomain that binds mitochondrial lipids selectively and releases cytochrome C.Cell death and differentiation · 2023Article
- Mitochondria and cell death-associated inflammation.Cell death and differentiation · 2023Review
- Bcl-2 Family Members and the Mitochondrial Import Machineries: The Roads to Death.Biomolecules · 2022Review
- The modified mitochondrial outer membrane carrier MTCH2 links mitochondrial fusion to lipogenesis.The Journal of cell biology · 2021Article
- NMR identification of a conserved Drp1 cardiolipin-binding motif essential for stress-induced mitochondrial fission.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Stepwise activation of the pro-apoptotic protein Bid at mitochondrial membranes.Cell death and differentiation · 2021Article
- Mechanistic connections between mitochondrial biology and regulated cell death.Developmental cell · 2021Review
- Mitochondrial outer membrane permeabilization at the single molecule level.Cellular and molecular life sciences : CMLS · 2021Review
- Membrane Transporters and Channels in Melanoma.Reviews of physiology, biochemistry and pharmacology · 2021Review
- MARCH5 requires MTCH2 to coordinate proteasomal turnover of the MCL1:NOXA complex.Cell death and differentiation · 2020Article
- Regulation of Mammalian Mitochondrial Dynamics: Opportunities and Challenges.Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During apoptosis, proapoptotic BAX and BAK trigger mitochondrial outer membrane (MOM) permeabilization by a mechanism that is not yet fully understood. BH3-only proteins such as tBID, together with lipids of the MOM, are thought to play a key role in BAX and BAK activation. In particular, cardiolipin (CL) has been shown to stimulate tBID-induced BAX activation in vitro. However, it is still unclear whether this process also relies on CL in the cell, or whether it is more dependent on MTCH2, a proposed receptor for tBID present in the MOM. To address this issue, we deleted both alleles of cardiolipin synthase in human HCT116 cells by homologous recombination, which resulted in a complete absence of CL. The CL-deficient cells were fully viable in glucose but displayed impaired oxidative phosphorylation and an inability to grow in galactose. Using these cells, we found that CL was not required for either tBID-induced BAX activation, or for apoptosis in response to treatment with TRAIL. Downregulation of MTCH2 in HCT116 cells also failed to prevent recruitment of tBID to mitochondria in apoptotic conditions. However, when both CL and MTCH2 were depleted, a significant reduction in tBID recruitment was observed, suggesting that in HCT116 cells, CL and MTCH2 can have redundant functions in this process.
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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.