ArticleJournal of cellular biochemistry2010
The 19S proteasomal lid subunit POH1 enhances the transcriptional activation by Mitf in osteoclasts.
Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- PSMD14-mediated deubiquitination of CARM1 facilitates the proliferation and metastasis of hepatocellular carcinoma by inducing the transcriptional activation of FERMT1.Cell death & disease · 2025Article
- Hypoxia Promotes Osteoclast Differentiation by Weakening USP18-Mediated Suppression on the NF-κB Signaling Pathway.International journal of molecular sciences · 2024Article
- PSMD14 is a novel prognostic marker and therapeutic target in osteosarcoma.Diagnostic pathology · 2024Article
- Article
- Structural and Functional Basis of JAMM Deubiquitinating Enzymes in Disease.Biomolecules · 2022Review
- The underestimated role of the microphthalmia-associated transcription factor (MiTF) in normal and pathological haematopoiesis.Cell & bioscience · 2021Review
- Deubiquitination of MITF-M Regulates Melanocytes Proliferation and Apoptosis.Frontiers in molecular biosciences · 2021Article
- The PSMD14 inhibitor Thiolutin as a novel therapeutic approach for esophageal squamous cell carcinoma through facilitating SNAIL degradation.Theranostics · 2021Article
- The deubiquitinating enzyme PSMD14 facilitates tumor growth and chemoresistance through stabilizing the ALK2 receptor in the initiation of BMP6 signaling pathway.EBioMedicine · 2019Article
- POH1 contributes to hyperactivation of TGF-β signaling and facilitates hepatocellular carcinoma metastasis through deubiquitinating TGF-β receptors and caveolin-1.EBioMedicine · 2019Article
- POH1 deubiquitinates pro-interleukin-1β and restricts inflammasome activity.Nature communications · 2018Article
- POH1 Knockdown Induces Cancer Cell Apoptosis via p53 and Bim.Neoplasia (New York, N.Y.) · 2018Article
- Deubiquitinating Enzymes and Bone Remodeling.Stem cells international · 2018Review
- Review
- Role of Deubiquitinating Enzymes in DNA Repair.Molecular and cellular biology · 2016Review
- POH1 deubiquitylates and stabilizes E2F1 to promote tumour formation.Nature communications · 2015Article
- Functions of the proteasome on chromatin.Biomolecules · 2014Review
- Diversity in genetic in vivo methods for protein-protein interaction studies: from the yeast two-hybrid system to the mammalian split-luciferase system.Microbiology and molecular biology reviews : MMBR · 2012Review
- Ubiquitin and proteasomes in transcription.Annual review of biochemistry · 2012Review
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The microphthalmia-associated transcription factor (Mitf) regulates gene expression required for osteoclast differentiation. Genes regulated by Mitf have been previously identified. However, proteins that interact and regulate Mitf's activity in osteoclasts are not well known. Here, we report that POH1, a subunit of the 19S proteasome lid is a regulator of Mitf. We show that POH1 and Mitf interact in osteoclasts and that this interaction is dependent on RANKL signaling. Overexpression of POH1 increased Mitf's activation of 5XGal4-TK and Acp5 promoters. The amino terminus of POH1 mediates the binding to Mitf and is sufficient to increase Mitf's transcriptional activity. Finally, we show that mutations in the JAMM motif of POH1 reduced Mitf activation of promoters. In summary, our results identify a novel mechanism of Mitf regulation in osteoclasts by POH1.
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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.