ArticleHuman molecular genetics2017
A conserved retromer sorting motif is essential for mitochondrial DLP1 recycling by VPS35 in Parkinson's disease model.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- A Quarter Century of EHD Protein Research: From Endosomal Recycling to Ciliopathies.Traffic (Copenhagen, Denmark) · 2026Review
- The Legionella effector RidL binds the large fission GTPase Drp1 to promote mitochondrial fragmentation.EMBO reports · 2026Article
- MAPL regulates gasdermin-mediated release of mtDNA from lysosomes to drive pyroptotic cell death.Nature cell biology · 2025Article
- A novel, rapidly progressive ataxia due to a spontaneous Myo5a mutation in mice impairs transport proteins and alters mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- Understanding the contributions of VPS35 and the retromer in neurodegenerative disease.Neurobiology of disease · 2022Review
- The retromer complex regulates C. elegans development and mammalian ciliogenesis.Journal of cell science · 2022Article
- C19orf12 ablation causes ferroptosis in mitochondrial membrane protein-associated with neurodegeneration.Free radical biology & medicine · 2022Article
- Retromer dependent changes in cellular homeostasis and Parkinson's disease.Essays in biochemistry · 2021Review
- De novo macrocyclic peptides for inhibiting, stabilizing, and probing the function of the retromer endosomal trafficking complex.Science advances · 2021Article
- Parkinson's disease-associated VPS35 mutant reduces mitochondrial membrane potential and impairs PINK1/Parkin-mediated mitophagy.Translational neurodegeneration · 2021Article
- The cell biology of Parkinson's disease.The Journal of cell biology · 2021Review
- PGC-1s in the Spotlight with Parkinson's Disease.International journal of molecular sciences · 2021Review
- Review
- Qualitative and Quantitative Assessment of the Role of Endocytic Regulatory and/or Rab Proteins on Mitochondrial Fusion and Fission.Methods in molecular biology (Clifton, N.J.) · 2021Article
- (D620N) VPS35 causes the impairment of Wnt/β-catenin signaling cascade and mitochondrial dysfunction in a PARK17 knockin mouse model.Cell death & disease · 2020Article
- RareBrain sciences · 2020Article
- Endocytic membrane trafficking in the control of centrosome function.Current opinion in cell biology · 2020Review
- Tollip coordinates Parkin-dependent trafficking of mitochondrial-derived vesicles.The EMBO journal · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Impaired mitochondria dynamics and quality control are involved in mitochondrial dysfunction and pathogenesis of Parkinson's disease (PD). VPS35 mutations cause autosomal dominant PD and we recently demonstrated that fPD-associated VPS35 mutants can cause mitochondrial fragmentation through enhanced VPS35-DLP1 interaction. In this study, we focused on the specific sites on DLP1 responsible for the VPS35-DLP1 interaction. A highly conserved FLV motif was identified in the C-terminus of DLP1, mutation of which significantly reduced VPS35-DLP1 interaction. A decoy peptide design based on this FLV motif could block the VPS35-DLP1 interaction and inhibit the recycling of mitochondrial DLP1 complexes. Importantly, VPS35 D620N mutant-induced mitochondrial fragmentation and respiratory deficits could be rescued by the treatment of this decoy peptide in both M17 cells overexpressing D620N or PD fibroblasts bearing this mutation. Overall, our results lend further support to the notion that VPS35-DLP1 interaction is key to the retromer-dependent recycling of mitochondrial DLP1 complex during mitochondrial fission and provide a novel therapeutic target to control excessive fission and associated mitochondrial deficits.
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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.