ArticleNature metabolism2023
COX17 acetylation via MOF-KANSL complex promotes mitochondrial integrity and function.
Article in Nature metabolism, 2023. 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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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
22 citing papers in PubMed, 32 citations in OpenAlex.
- Rab1A Promotes Hepatic Steatosis by Suppressing Mitophagy via the Raf-1/ERK1/2/PINK1 Signaling Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- Higher-order structural organization of mitochondrial metabolism.The Journal of biological chemistry · 2026Review
- Lactylation and acetylation: parallel paths, divergent deeds, and research dilemmas.Journal of translational medicine · 2026Review
- Nucleoli-localized KANSL2 as an epigenetic regulator of ribosome biogenesis in glioblastoma cells.Communications biology · 2026Article
- BLOC1S1 depletion via splice-switching oligonucleotides improves mitochondrial respiration and rescues ALS phenotypes.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Review
- β-Hydroxybutyrate-induced mitochondrial dysfunction and oxidative stress in BMSCs are ameliorated by mitophagy activation.Frontiers in cell and developmental biology · 2026Article
- Polycomb Repressive Complex 1 and USP16 localize to the mitochondrion and influence its function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cardiomyocyte lncRNA Cpat maintains cardiac homeostasis and mitochondria function by targeting citrate synthase acetylation.Nature communications · 2025Article
- TRAP1 inhibits KANSL3 acetylation to alleviate mitochondrial dysfunction by promoting mitophagy in cardiomyocytes under diabetic conditions.Cell communication and signaling : CCS · 2025Article
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
- A-485 alleviates postmenopausal osteoporosis by activating GLUD1 deacetylation through the SENP1-Sirt3 signal pathway.Journal of orthopaedic surgery and research · 2025Article
- Post-translational modifications and the reprogramming of tumor metabolism.Discover oncology · 2025Review
- Obstructive Sleep Apnea and Parkinson's Disease: Bidirectional Clinical and Pathophysiologic Links.International journal of molecular sciences · 2025Review
- KAT8 facilitates the proliferation of cancer cells through enhancing E7 function in HPV-associated cervical cancer.Acta biochimica et biophysica Sinica · 2025Article
- Investigating Potential Biomarkers of Ankylosing Spondylitis: A Study on Mitochondrial and Senescence Pathways Using Machine Learning.Journal of inflammation research · 2025Article
- Deciphering the role of sphingolipid metabolism in the immune microenvironment and prognosis of esophageal cancer via single-cell sequencing and bulk data analysis.Discover oncology · 2024Article
- Acetyl-CoA synthetase activity is enzymatically regulated by lysine acetylation using acetyl-CoA or acetyl-phosphate as donor molecule.Nature communications · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Reversible acetylation of mitochondrial proteins is a regulatory mechanism central to adaptive metabolic responses. Yet, how such functionally relevant protein acetylation is achieved remains unexplored. Here we reveal an unprecedented role of the MYST family lysine acetyltransferase MOF in energy metabolism via mitochondrial protein acetylation. Loss of MOF-KANSL complex members leads to mitochondrial defects including fragmentation, reduced cristae density and impaired mitochondrial electron transport chain complex IV integrity in primary mouse embryonic fibroblasts. We demonstrate COX17, a complex IV assembly factor, as a bona fide acetylation target of MOF. Loss of COX17 or expression of its non-acetylatable mutant phenocopies the mitochondrial defects observed upon MOF depletion. The acetylation-mimetic COX17 rescues these defects and maintains complex IV activity even in the absence of MOF, suggesting an activatory role of mitochondrial electron transport chain protein acetylation. Fibroblasts from patients with MOF syndrome who have intellectual disability also revealed respiratory defects that could be restored by alternative oxidase, acetylation-mimetic COX17 or mitochondrially targeted MOF. Overall, our findings highlight the critical role of MOF-KANSL complex in mitochondrial physiology and provide new insights into MOF syndrome.
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Registered trials
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.