ArticleCell death & disease2021
Ubiquitin-specific protease 53 promotes osteogenic differentiation of human bone marrow-derived mesenchymal stem cells.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- Histopathological Analysis of Adipose-Derived Mesenchymal Stem Cells and Their Osteogenic Derivatives in Promoting Bone Regeneration in a Model of Fracture Nonunion.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026Article
- Integrated stress response genes as novel biomarkers and therapeutic targets in ankylosing spondylitis: a transcriptomic and Mendelian randomization study.Frontiers in immunology · 2026Article
- PERRC: Protease Engineering with Reactant Residence Time Control.ACS synthetic biology · 2025Article
- EIF4A3 enhances the viability, invasion and osteogenic differentiation of BMSCs via the USP53/SMAD5 pathway.Scientific reports · 2025Article
- Regulatory Roles of E3 Ubiquitin Ligases and Deubiquitinases in Bone.Biomolecules · 2025Review
- Review
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377.Research (Washington, D.C.) · 2025Article
- Role of ubiquitination in the occurrence and development of osteoporosis (Review).International journal of molecular medicine · 2024Review
- 3'-Sialyllactose alleviates bone loss by regulating bone homeostasis.Communications biology · 2024Article
- Article
- Endothelial Dickkopf-1 Promotes Smooth Muscle Cell-derived Foam Cell Formation via USP53-mediated Deubiquitination of SR-A During Atherosclerosis.International journal of biological sciences · 2024Article
- An Overview of the Deubiquitinase USP53: A Promising Diagnostic Marker and Therapeutic Target.Current protein & peptide science · 2024Review
- USP53 Exerts Tumor-Promoting Effects in Triple-Negative Breast Cancer by Deubiquitinating CRKL.Cancers · 2023Article
- Ubiquitin-specific peptidases: Players in bone metabolism.Cell proliferation · 2023Review
- Strategies of Macrophages to Maintain Bone Homeostasis and Promote Bone Repair: A Narrative Review.Journal of functional biomaterials · 2022Review
- RNF4~RGMb~BMP6 axis required for osteogenic differentiation and cancer cell survival.Cell death & disease · 2022Article
- Deubiquitinating Enzyme USP7 Is Required for Self-Renewal and Multipotency of Human Bone Marrow-Derived Mesenchymal Stromal Cells.International journal of molecular sciences · 2022Article
- USP53 plays an antitumor role in hepatocellular carcinoma through deubiquitination of cytochrome c.Oncogenesis · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ubiquitin protease pathway plays important role in human bone marrow-derived mesenchymal stem cell (hBMSC) differentiation, including osteogenesis. However, the function of deubiquitinating enzymes in osteogenic differentiation of hBMSCs remains poorly understood. In this study, we aimed to investigate the role of ubiquitin-specific protease 53 (USP53) in the osteogenic differentiation of hBMSCs. Based on re-analysis of the Gene Expression Omnibus database, USP53 was selected as a positive regulator of osteogenic differentiation in hBMSCs. Overexpression of USP53 by lentivirus enhanced osteogenesis in hBMSCs, whereas knockdown of USP53 by lentivirus inhibited osteogenesis in hBMSCs. In addition, USP53 overexpression increased the level of active β-catenin and enhanced the osteogenic differentiation of hBMSCs. This effect was reversed by the Wnt/β-catenin inhibitor DKK1. Mass spectrometry showed that USP53 interacted with F-box only protein 31 (FBXO31) to promote proteasomal degradation of β-catenin. Inhibition of the osteogenic differentiation of hBMSCs by FBXO31 was partially rescued by USP53 overexpression. Animal studies showed that hBMSCs with USP53 overexpression significantly promoted bone regeneration in mice with calvarial defects. These results suggested that USP53 may be a target for gene therapy for bone regeneration.
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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 Socratic graph.