ArticleThe EMBO journal2016
Loss of FBXO7 (PARK15) results in reduced proteasome activity and models a parkinsonism-like phenotype in mice.
Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- The Emerging Roles of E3 Ligases and DUBs in Neurodegenerative Diseases.Molecular neurobiology · 2023Pooled it
- Structural basis for regulation of the proteasome 20S core particle by the Parkinsonism-associated proteins FBXO7 and PI31.bioRxiv : the preprint server for biology · 2026Article
- rAAV Fbxo7 gene therapy rescues the progressive nigrostriatal pathology in a mouse model of juvenile parkinsonism.Acta neuropathologica communications · 2026Article
- Variants in the proteasome regulator PSMF1 cause a phenotypic spectrum from parkinsonism to perinatal lethality.Nature communications · 2026Article
- PI31 expression is neuroprotective in a mouse model of early-onset parkinsonism.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- FBXO7 ubiquitinates PRMT1 to suppress serine synthesis and tumor growth in hepatocellular carcinoma.Nature communications · 2024Article
- FBXO7 Confers Mesenchymal Properties and Chemoresistance in Glioblastoma by Controlling Rbfox2-Mediated Alternative Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- PARK15/FBXO7 is dispensable for PINK1/Parkin mitophagy in iNeurons and HeLa cell systems.EMBO reports · 2023Article
- Identification of Potential Biomarkers for Diagnosis of Patients with Methamphetamine Use Disorder.International journal of molecular sciences · 2023Article
- Dynamic Metabolic and Transcriptional Responses of Proteasome-Inhibited Neurons.Antioxidants (Basel, Switzerland) · 2023Article
- USP7 attenuates endoplasmic reticulum stress-induced apoptotic cell death through deubiquitination and stabilization of FBXO7.PloS one · 2023Article
- Impaired mitochondrial accumulation and Lewy pathology in neuron-specific FBXO7-deficient mice.Molecular brain · 2022Article
- FBXO7 triggers caspase 8-mediated proteolysis of the transcription factor FOXO4 and exacerbates neuronal cytotoxicity.The Journal of biological chemistry · 2021Article
- Animal Models of Autosomal Recessive Parkinsonism.Biomedicines · 2021Review
- Analysis of the FBXO7 promoter reveals overlapping Pax5 and c-Myb binding sites functioning in B cells.Biochemical and biophysical research communications · 2021Article
- The Pathogenesis of Parkinson's Disease: A Complex Interplay Between Astrocytes, Microglia, and T Lymphocytes?Frontiers in neurology · 2021Review
- Low-Expressing Synucleinopathy Mouse Models Based on Oligomer-Forming Mutations and C-Terminal Truncation of α-Synuclein.Frontiers in neuroscience · 2021Article
- Article
- Review
- Machine learning discriminates a movement disorder in a zebrafish model of Parkinson's disease.Disease models & mechanisms · 2020Article
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Mutations in the FBXO7 (PARK15) gene have been implicated in a juvenile form of parkinsonism termed parkinsonian pyramidal syndrome (PPS), characterized by Parkinsonian symptoms and pyramidal tract signs. FBXO7 (F-box protein only 7) is a subunit of the SCF (SKP1/cullin-1/F-box protein) E3 ubiquitin ligase complex, but its relevance and function in neurons remain to be elucidated. Here, we report that the E3 ligase FBXO7-SCF binds to and ubiquitinates the proteasomal subunit PSMA2. In addition, we show that FBXO7 is a proteasome-associated protein involved in proteasome assembly. In FBXO7 knockout mice, we find reduced proteasome activity and early-onset motor deficits together with premature death. In addition, we demonstrate that NEX (neuronal helix-loop-helix protein-1)-Cre-induced deletion of the FBXO7 gene in forebrain neurons or the loss of FBXO7 in tyrosine hydroxylase (TH)-positive neurons results in motor defects, reminiscent of the phenotype in PARK15 patients. Taken together, our study establishes a vital role for FBXO7 in neurons, which is required for proper motor control and accentuates the importance of FBXO7 in proteasome function.
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