ArticleJournal of immunology (Baltimore, Md. : 1950)2015
PRL-3 mediates the protein maturation of ULBP2 by regulating the tyrosine phosphorylation of HSP60.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- PRL-3: unveiling a new horizon in cancer therapy.Acta pharmacologica Sinica · 2025Review
- Molecular Chaperonin HSP60: Current Understanding and Future Prospects.International journal of molecular sciences · 2024Review
- Interleukin-30 subverts prostate cancer-endothelium crosstalk by fostering angiogenesis and activating immunoregulatory and oncogenic signaling pathways.Journal of experimental & clinical cancer research : CR · 2023Article
- De novo CLPTM1 variants with reduced GABAEpilepsia · 2023Article
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Hsp60 Post-translational Modifications: Functional and Pathological Consequences.Frontiers in molecular biosciences · 2020Review
- Phosphoproteins Involved in the Inhibition of Apoptosis and in Cell Survival in the Leiomyoma.Journal of clinical medicine · 2019Article
- Roles of astrocytic connexin-43, hemichannels, and gap junctions in oxygen-glucose deprivation/reperfusion injury induced neuroinflammation and the possible regulatory mechanisms of salvianolic acid B and carbenoxolone.Journal of neuroinflammation · 2018Article
- HSP60 possesses a GTPase activity and mediates protein folding with HSP10.Scientific reports · 2017Article
- PRL3-zumab, a first-in-class humanized antibody for cancer therapy.JCI insight · 2016Article
- Intracellular antigens as targets for antibody based immunotherapy of malignant diseases.Molecular oncology · 2015Review
- Comprehensive Analysis of lncRNA-miRNA- mRNA Network Ascertains Prognostic Factors in Patients with Colon Cancer.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Many malignant cells release the NKG2D ligand ULBP2 from their cell surface to evade immunosurveillance by NK cells and CD8 T cells. Although the shedding mechanism remains unclear, various inhibitors of matrix metalloproteinases have been shown to efficiently block the release of soluble ULBP2. The clinical use of these inhibitors, however, is limited because of adverse side effects. Using high-throughput screening technique, we identified a specific inhibitor of phosphatase of regenerating liver 3 (PRL-3) that could reduce the level of soluble ULBP2 in the culture supernatant of various cancer cell lines. Inhibition or gene knockdown of PRL-3 did not reduce ULBP2 shedding, but rather suppressed posttranslational maturation of ULBP2, resulting in intracellular retention of immature ULBP2. We then found that ULBP2 was constitutively associated with heat shock protein HSP60. Complete maturation of ULBP2 required tyrosine phosphorylation of HSP60 which was mediated by PRL-3.
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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.