ArticleMolecular and cellular biology2010
Inhibition of human peptide deformylase disrupts mitochondrial function.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
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
23 citing papers in PubMed, 48 citations in OpenAlex.
- Sprint interval exercise disrupts mitochondrial ultrastructure driving a unique mitochondrial stress response and remodelling in men.Nature communications · 2025Trial
- N-terminal formylmethionine as a degron and a specific signal in proteostasis and stress adaptation.Experimental & molecular medicine · 2026Review
- Vacuolar-type HNature communications · 2025Article
- Hypoxia-induced tRF-3Frontiers in pharmacology · 2025Article
- Cytosolic N-terminal formyl-methionine deformylation derives cancer stem cell features and tumor progression.Scientific reports · 2024Article
- Harnessing the cyclization strategy for new drug discovery.Acta pharmaceutica Sinica. B · 2022Review
- System-wide analyses reveal essential roles of N-terminal protein modification in bacterial membrane integrity.iScience · 2022Article
- Mechanisms and regulation of protein synthesis in mitochondria.Nature reviews. Molecular cell biology · 2021Review
- Targeting Mitochondrial Protein Expression as a Future Approach for Cancer Therapy.Frontiers in oncology · 2021Review
- Maternally inherited peptides as strain-specific chemosignals.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Targeting Endothelial Barrier Dysfunction Caused by Circulating Bacterial and Mitochondrial N-Formyl Peptides With Deformylase.Frontiers in immunology · 2019Article
- Mitochondrial ribosomes in cancer.Seminars in cancer biology · 2017Review
- A unique peptide deformylase platform to rationally design and challenge novel active compounds.Scientific reports · 2016Article
- Structure-Based Drug Design of Small Molecule Peptide Deformylase Inhibitors to Treat Cancer.Molecules (Basel, Switzerland) · 2016Article
- Quality control of mitochondrial protein synthesis is required for membrane integrity and cell fitness.The Journal of cell biology · 2015Article
- Integrating mitochondrial translation into the cellular context.Nature reviews. Molecular cell biology · 2015Review
- The role of formylated peptides and formyl peptide receptor 1 in governing neutrophil function during acute inflammation.The American journal of pathology · 2015Review
- Inhibition of human mitochondrial peptide deformylase causes apoptosis in c-myc-overexpressing hematopoietic cancers.Cell death & disease · 2014Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Deformylases are metalloproteases in bacteria, plants, and humans that remove the N-formyl-methionine off peptides in vitro. The human homolog of peptide deformylase (HsPDF) resides in the mitochondria, along with its putative formylated substrates; however, the cellular function of HsPDF remains elusive. Here we report on the function of HsPDF in mitochondrial translation and oxidative phosphorylation complex biogenesis. Functional HsPDF appears to be necessary for the accumulation of mitochondrial DNA-encoded proteins and assembly of new respiratory complexes containing these proteins. Consequently, inhibition of HsPDF reduces respiratory function and cellular ATP levels, causing dependence on aerobic glycolysis for cell survival. A series of structurally different HsPDF inhibitors and control peptidase inhibitors confirmed that inhibition of HsPDF decreases mtDNA-encoded protein accumulation. Therefore, HsPDF appears to have a role in maintenance of mitochondrial respiratory function, and this function is analogous to that of chloroplast PDF.
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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.