ArticleCell death & disease2013
Drosophila Trap1 protects against mitochondrial dysfunction in a PINK1/parkin model of Parkinson's disease.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 129 citations in OpenAlex.
- Rewiring Lipid Metabolism: PINK1 as a Central Regulator of Mitochondrial Homeostasis in Parkinson's Disease.International journal of molecular sciences · 2026Review
- 5-ALA/SFC Mitigates Tau Toxicity via Lowering Oxidative Stress in aLife (Basel, Switzerland) · 2026Article
- TRAP1 and its therapeutic potential.Bioorganic & medicinal chemistry letters · 2025Review
- The Mitochondrial Hsp90 HomologInsects · 2025Article
- A Drosophila model of prion disease and its metabolic changes in the brain.Animal models and experimental medicine · 2025Article
- Point mutations of the mitochondrial chaperone TRAP1 affect its functions and pro-neoplastic activity.Cell death & disease · 2025Article
- Oral administration of aripiprazole to Drosophila causes intestinal toxicity.Disease models & mechanisms · 2025Article
- Parkinson's disease and glucose metabolism impairment.Translational neurodegeneration · 2025Review
- TRAP1 functions in the morphogenesis of the embryonic kidney.Animal cells and systems · 2025Article
- TRAP1 drives smooth muscle cell senescence and promotes atherosclerosis via HDAC3-primed histone H4 lysine 12 lactylation.European heart journal · 2024Article
- Verbascoside Elicits Its Beneficial Effects by Enhancing Mitochondrial Spare Respiratory Capacity and the Nrf2/HO-1 Mediated Antioxidant System in a Murine Skeletal Muscle Cell Line.International journal of molecular sciences · 2023Article
- IFI27 Integrates Succinate and Fatty Acid Oxidation to Promote Adipocyte Thermogenic Adaption.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The antipsychotic medications aripiprazole, brexpiprazole and cariprazine are off-target respiratory chain complex I inhibitors.Biology direct · 2023Article
- Caffeine improves mitochondrial function in PINK1Journal of bioenergetics and biomembranes · 2023Article
- Post-translational modification and mitochondrial function in Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
- The development of cancers research based on mitochondrial heat shock protein 90.Frontiers in oncology · 2023Review
- Activation of mitochondrial TRAP1 stimulates mitochondria-lysosome crosstalk and correction of lysosomal dysfunction.iScience · 2022Article
- The Mitochondrial HSP90 Paralog TRAP1: Structural Dynamics, Interactome, Role in Metabolic Regulation, and Inhibitors.Biomolecules · 2022Review
- TRAP1 Chaperones the Metabolic Switch in Cancer.Biomolecules · 2022Review
- Enhanced Expression of TRAP1 Protects Mitochondrial Function in Motor Neurons under Conditions of Oxidative Stress.International journal of molecular sciences · 2022Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction caused by protein aggregation has been shown to have an important role in neurological diseases, such as Parkinson's disease (PD). Mitochondria have evolved at least two levels of defence mechanisms that ensure their integrity and the viability of their host cell. First, molecular quality control, through the upregulation of mitochondrial chaperones and proteases, guarantees the clearance of damaged proteins. Second, organellar quality control ensures the clearance of defective mitochondria through their selective autophagy. Studies in Drosophila have highlighted mitochondrial dysfunction linked with the loss of the PTEN-induced putative kinase 1 (PINK1) as a mechanism of PD pathogenesis. The mitochondrial chaperone TNF receptor-associated protein 1 (TRAP1) was recently reported to be a cellular substrate for the PINK1 kinase. Here, we characterise Drosophila Trap1 null mutants and describe the genetic analysis of Trap1 function with Pink1 and parkin. We show that loss of Trap1 results in a decrease in mitochondrial function and increased sensitivity to stress, and that its upregulation in neurons of Pink1 mutant rescues mitochondrial impairment. Additionally, the expression of Trap1 was able to partially rescue mitochondrial impairment in parkin mutant flies; and conversely, expression of parkin rescued mitochondrial impairment in Trap1 mutants. We conclude that Trap1 works downstream of Pink1 and in parallel with parkin in Drosophila, and that enhancing its function may ameliorate mitochondrial dysfunction and rescue neurodegeneration in PD.
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