ArticleInternational journal of biological sciences2007
Silencing of the Pink1 gene expression by conditional RNAi does not induce dopaminergic neuron death in mice.
Article in International journal of biological sciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 98 citations in OpenAlex.
- Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026Review
- Cellular stress, cell death, and extracellular vesicles: redefining the therapeutic landscape of rheumatoid arthritis.Clinical rheumatology · 2026Review
- Bone morphogenetic protein 4-associated mitochondrial dysfunction in diabetic nephropathy involves Parkin downregulation.Frontiers in clinical diabetes and healthcare · 2026Article
- Insights into PINK1/Parkin function and dysfunction from Drosophila models.The Biochemical journal · 2025Review
- Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025Review
- Behavioral analysis of motor and non-motor impairment in rodent models of Parkinson's disease.Frontiers in aging neuroscience · 2024Review
- PINK1-PRKN mediated mitophagy: differences betweenAutophagy · 2023Review
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- New pathogenic insights from large animal models of neurodegenerative diseases.Protein & cell · 2022Review
- Urolithin A attenuates auditory cell senescence by activating mitophagy.Scientific reports · 2022Article
- A Critical Review of Zebrafish Models of Parkinson's Disease.Frontiers in pharmacology · 2022Review
- PTEN-Induced Putative Kinase 1 Dysfunction Accelerates Synucleinopathy.Journal of Parkinson's disease · 2022Article
- Genetically modified large animal models for investigating neurodegenerative diseases.Cell & bioscience · 2021Review
- Animal Models of Autosomal Recessive Parkinsonism.Biomedicines · 2021Review
- Shedding light on mitophagy in neurons: what is the evidence for PINK1/Parkin mitophagy in vivo?Cellular and molecular life sciences : CMLS · 2018Review
- Parkin and PINK1 functions in oxidative stress and neurodegeneration.Brain research bulletin · 2017Review
- PINK1 Primes Parkin-Mediated Ubiquitination of PARIS in Dopaminergic Neuronal Survival.Cell reports · 2017Article
- Mouse Genetic Models of Human Brain Disorders.Frontiers in genetics · 2016Review
- Defining functional gene-circuit interfaces in the mouse nervous system.Genes, brain, and behavior · 2014Review
- Gudu, an Armadillo repeat-containing protein, is required for spermatogenesis in Drosophila.Gene · 2013Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Transgenic RNAi, an alternative to the gene knockout approach, can induce hypomorphic phenotypes that resemble those of the gene knockout in mice. Conditional transgenic RNAi is an attractive choice of method for reverse genetics in vivo because it can achieve temporal and spatial silencing of targeted genes. Pol III promoters such as U6 are widely used to drive the expression of RNAi transgenes in animals. Tested in transgenic mice, a Cre-loxP inducible U6 promoter drove the broad expression of an shRNA against the Pink1 gene whose loss-of-functional mutations cause one form of familial Parkinson's disease. The expression of the shRNA was tightly regulated and, when induced, silenced the Pink1 gene product by more than 95% in mouse brain. However, these mice did not develop dopaminergic neurodegeneration, suggesting that silencing of the Pink1 gene expression from embryo in mice is insufficient to cause similar biochemical or morphological changes that are observed in Parkinson's disease. The results demonstrate that silencing of the PINK1 gene does not induce a reliable mouse model for Parkinson's disease, but that technically the inducible U6 promoter is useful for conditional RNAi in vivo.
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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.