ArticleScientific reports2021
Drosophila tubulin polymerization promoting protein mutants reveal pathological correlates relevant to human Parkinson's disease.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Insights from TPPP3 and its family member proteins in neuronal diseases.Neural regeneration research · 2026Article
- Variants in the proteasome regulator PSMF1 cause a phenotypic spectrum from parkinsonism to perinatal lethality.Nature communications · 2026Article
- Conserved Pathways, Divergent Outcomes: A Cross-Species Genomic Perspective on the Cancer-Neurodegeneration Paradox.International journal of molecular sciences · 2026Review
- In Vivo Screen of Parkinson's Disease GWAS Risk Genes IdentifiesThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- OTUD6A drives dopaminergic neuronal degeneration of Parkinson's disease through deubiquitinating ACTG1 in neuronal cells.Acta pharmaceutica Sinica. B · 2026Article
- Tubulin Polymerization Promoting Proteins: Functional Diversity With Implications in Neurological Disorders.Journal of neuroscience research · 2025Review
- Perspective Strategies for Interventions in Parkinsonism: Remedying the Neglected Role of TPPP.Cells · 2024Article
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- Article
- Modulatory Role of TPPP3 in Microtubule Organization and Its Impact on Alpha-Synuclein Pathology.Cells · 2022Article
- Intrinsic maturation of sleep output neurons regulates sleep ontogeny in Drosophila.Current biology : CB · 2022Article
- Article
- Will Sirtuin 2 Be a Promising Target for Neuroinflammatory Disorders?Frontiers in cellular neuroscience · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder with no known cure. PD is characterized by locomotion deficits, nigrostriatal dopaminergic neuronal loss, mitochondrial dysfunctions and formation of α-Synuclein aggregates. A well-conserved and less understood family of Tubulin Polymerization Promoting Proteins (TPPP) is also implicated in PD and related disorders, where TPPP exists in pathological aggregates in neurons in patient brains. However, there are no in vivo studies on mammalian TPPP to understand the genetics and neuropathology linking TPPP aggregation or neurotoxicity to PD. Recently, we discovered the only Drosophila homolog of human TPPP named Ringmaker (Ringer). Here, we report that adult ringer mutants display progressive locomotor disabilities, reduced lifespan and neurodegeneration. Importantly, our findings reveal that Ringer is associated with mitochondria and ringer mutants have mitochondrial structural damage and dysfunctions. Adult ringer mutants also display progressive loss of dopaminergic neurons. Together, these phenotypes of ringer mutants recapitulate some of the salient features of human PD patients, thus allowing us to utilize ringer mutants as a fly model relevant to PD, and further explore its genetic and molecular underpinnings to gain insights into the role of human TPPP in PD.
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