ArticleScientific reports2017
Midnolin is a novel regulator of parkin expression and is associated with Parkinson's Disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- CHCHD2 and CHCHD10 promoted autophagic clearance of protein aggregates via GABARAPs.Autophagy · 2026Article
- Exploring the sex-dependent effects of midnolin loss on hepatic transcription and chromatin accessibility.Biochemistry and biophysics reports · 2026Article
- Proteasomal control of transcription factors: mechanisms, regulation and dysregulation.Cellular and molecular life sciences : CMLS · 2026Review
- RNF126 writes a non-canonical ubiquitin code on midnolin to tune protein stability.Acta biochimica et biophysica Sinica · 2026Article
- Emerging roles of Midnolin in Cancer, Parkinson's Disease, and Metabolic dysfunction.Molecular biology reports · 2025Review
- Targeting GSK3β and signaling pathways in breast cancer: role of individual members of miR- 23/24/27 cluster.BMC cancer · 2025Article
- 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
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- 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
- Heterozygous midnolin knockout attenuates severity of nonalcoholic fatty liver disease in mice fed a Western-style diet high in fat, cholesterol, and fructose.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- CRISPR/Cas9 assisted stem cell therapy in Parkinson's disease.Biomaterials research · 2023Review
- Bioinformatics Analysis of Next Generation Sequencing Data Identifies Molecular Biomarkers Associated With Type 2 Diabetes Mellitus.Clinical medicine insights. Endocrinology and diabetes · 2023Article
- Article
- A cerebrospinal fluid microRNA analysis: Progressive supranuclear palsy.Molecular medicine reports · 2022Article
- Research on a Weighted Gene Co-expression Network Analysis method for mining pathogenic genes in thyroid cancer.PloS one · 2022Article
- Weighted gene co-expression network analysis identified underlying hub genes and mechanisms in the occurrence and development of viral myocarditis.Annals of translational medicine · 2020Article
- MIDN locus structural variants and Parkinson's Disease risk.Annals of clinical and translational neurology · 2020Article
- Reply to: MIDN locus structural variants and Parkinson's disease risk.Annals of clinical and translational neurology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Midnolin (MIDN) was first discovered in embryonic stem cells, but its physiological and pathological roles are, to date, poorly understood. In the present study, we therefore examined the role of MIDN in detail. We found that in PC12 cells, a model of neuronal cells, MIDN localized primarily to the nucleus and intracellular membranes. Nerve growth factor promoted MIDN gene expression, which was attenuated by specific inhibitors of extracellular signal-regulated kinases 1/2 and 5. MIDN-deficient PC12 cells created using CRISPR/Cas9 technology displayed significantly impaired neurite outgrowth. Interestingly, a genetic approach revealed that 10.5% of patients with sporadic Parkinson's disease (PD) had a lower MIDN gene copy number whereas no copy number variation was observed in healthy people, suggesting that MIDN is involved in PD pathogenesis. Furthermore, the expression of parkin, a major causative gene in PD, was significantly reduced by CRISPR/Cas9 knockout and siRNA knockdown of MIDN. Activating transcription factor 4 (ATF4) was also down-regulated, which binds to the cAMP response element (CRE) in the parkin core promoter region. The activity of CRE was reduced following MIDN loss. Overall, our data suggests that MIDN promotes the expression of parkin E3 ubiquitin ligase, and that MIDN loss can trigger PD-related pathogenic mechanisms.
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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.