ArticleJournal of cell science2014
CKMT1 regulates the mitochondrial permeability transition pore in a process that provides evidence for alternative forms of the complex.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
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- It Is Not Just About Storing Energy: The Multifaceted Role of Creatine Metabolism on Cancer Biology and Immunology.International journal of molecular sciences · 2024Review
- Social fear extinction susceptibility is associated with Microbiota-Gut-Brain axis alterations.Brain, behavior, and immunity · 2024Article
- Context-dependent roles for ubiquitous mitochondrial creatine kinase CKMT1 in breast cancer progression.Cell reports · 2024Article
- Mitochondrial control of microglial phagocytosis by the translocator protein and hexokinase 2 in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Multi-Targeting Intranasal Nanoformulation as a Therapeutic for Alzheimer's Disease.Biomolecules · 2023Article
- Molecular mechanisms and consequences of mitochondrial permeability transition.Nature reviews. Molecular cell biology · 2022Review
- A dual druggable genome-wide siRNA and compound library screening approach identifies modulators of parkin recruitment to mitochondria.The Journal of biological chemistry · 2020Article
- Single-walled carbon nanohorn aggregates promotes mitochondrial dysfunction-induced apoptosis in hepatoblastoma cells by targeting SIRT3.International journal of oncology · 2018Article
- ING5 differentially regulates protein lysine acetylation and promotes p300 autoacetylation.Oncotarget · 2018Article
- The Mitochondrial Permeability Transition Pore and ATP Synthase.Handbook of experimental pharmacology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The permeability transition pore (PT-pore) mediates cell death through the dissipation of the mitochondrial membrane potential (ΔΨm). Because the exact composition of the PT-pore is controversial, it is crucial to investigate the actual molecular constituents and regulators of this complex. We found that mitochondrial creatine kinase-1 (CKMT1) is a universal and functionally necessary gatekeeper of the PT-pore, as its depletion induces mitochondrial depolarization and apoptotic cell death. This can be inhibited efficiently by bongkrekic acid, a compound that is widely used to inhibit the PT-pore. However, when the 'classical' PT-pore subunits cyclophilin D and VDAC1 are pharmacologically inhibited or their expression levels reduced, mitochondrial depolarization by CKMT1 depletion remains unaffected. At later stages of drug-induced apoptosis, CKMT1 levels are reduced, suggesting that CKMT1 downregulation acts to reinforce the commitment of cells to apoptosis. A novel high-molecular-mass CKMT1 complex that is distinct from the known CKMT1 octamer disintegrates upon treatment with cytotoxic drugs, concomitant with mitochondrial depolarization. Our study provides evidence that CKMT1 is a key regulator of the PT-pore through a complex that is distinct from the classical PT-pore.
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Registered trials
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