ArticleAnnals of clinical and translational neurology2019
Midnolin is a confirmed genetic risk factor for Parkinson's disease.
Article in Annals of clinical and translational neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Midnolin Correlates With Anti-Tumour Immunity and Promotes Liver Cancer Progression Through β-Catenin.Journal of cellular and molecular medicine · 2025Article
- Comprehensive Analysis Reveals Midnolin as a Potential Prognostic, Therapeutic, and Immunological Cancer Biomarker.Biomedicines · 2025Article
- Viable mutations of mouse midnolin suppress B cell malignancies.The Journal of experimental medicine · 2024Article
- Midnolin, a Genetic Risk Factor for Parkinson's Disease, Promotes Neurite Outgrowth Accompanied by Early Growth Response 1 Activation in PC12 Cells.Molecular and cellular biology · 2024Article
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- A risk prognostic model for patients with esophageal squamous cell carcinoma basing on cuproptosis and ferroptosis.Journal of cancer research and clinical oncology · 2023Article
- Article
- A cerebrospinal fluid microRNA analysis: Progressive supranuclear palsy.Molecular medicine reports · 2022Article
- Reply to: MIDN locus structural variants and Parkinson's disease risk.Annals of clinical and translational neurology · 2020Article
- MIDN locus structural variants and Parkinson's Disease risk.Annals of clinical and translational neurology · 2020Article
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5 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveGenetic analysis of patients with familial Parkinson's disease (PD) identified many causative genes. However, the majority of PD cases are sporadic, and the mechanisms of onset still remain unclear. Previously, we found that Midnolin (MIDN) is associated with PD in a Yamagata (Japan) cohort study and that MIDN regulates neurite outgrowth and Parkin expression in neuronal cells. In the present study, we aimed to replicate the genetic association between MIDN and PD in a large British population cohort.
methodsIn this replication study, we analyzed the copy number variations and single-nucleotide polymorphisms of the MIDN gene in a large British population on a case-control genome-wide association study dataset including 2,860 controls and 2,168 PD patients.
resultsThere was significant copy number loss in the MIDN gene with an odds ratio of 4.35 (P < 2.2 × 10
interpretationWe showed the strong genetic association of MIDN with PD development in a British population and in a Japanese population, suggesting MIDN is a confirmed and universal genetic risk factor for PD.
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