ArticleMolecules and cells2012
A novel accessory molecule Trim59 involved in cytotoxicity of BCG-activated macrophages.
Article in Molecules and cells, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Prognostic significance of TRIM59 for cancer patient survival: A systematic review and meta-analysis.Medicine · 2019Pooled it
- TRIM59 deficiency promotes M1 macrophage activation and inhibits colorectal cancer through the STAT1 signaling pathway.Scientific reports · 2024Article
- Genome-wide analysis of genes encoding core components of the ubiquitin system during cerebral cortex development.Molecular brain · 2022Article
- The role of HIF-1α in BCG-stimulated macrophages polarization and their tumoricidal effects in vitro.Medical microbiology and immunology · 2021Article
- TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages through JNK signaling pathway.Cellular signalling · 2020Article
- TRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages.Frontiers in immunology · 2020Article
- TRIM59 loss in M2 macrophages promotes melanoma migration and invasion by upregulating MMP-9 and Madcam1.Aging · 2019Article
- Myositis in Lewis rats induced by the superantigen Staphylococcal enterotoxin A.Molecular biology reports · 2019Article
- Embryonic lethality in mice lacking Trim59 due to impaired gastrulation development.Cell death & disease · 2018Article
- PI3K/Akt signaling pathway modulates influenza virus induced mouse alveolar macrophage polarization to M1/M2b.PloS one · 2014Article
- Immunomodulatory effects of interferons in malignancies.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCG-activated macrophages (BAM) could kill the tumor cells through cell-cell contact. In this process membrane proteins play an important role. However, up to date, few membrane proteins were revealed. In this study, we selected a surface molecule named Trim59, which was specifically expressed on BAM membrane (compared with the negative control). We cloned and prokaryoticly expressed the extracellular domain of Trim59, purified the recombinant protein and generated polyclonal antibodies. Immunohistochemistry showed that Trim59 abundantly expressed in spleen, stomach and ovary; intermediately expressed in brain, lung, kidney, muscle and intestine; but not in thymus, liver, heart, uterus. Using the antibodies to block Trim59 on BAM significantly reduced BAM cytotoxicity against MCA207 cells. This demonstrated that Trim59 serves as an indispensable molecule in maintaining BAM activity. Overexpression of Trim59 in Raw264.7 cell line failed to lyse target MCA207 cells, which potentiated Trim59 per se could not enhance macrophage cytotoxicity; on another hand, overexpression of Trim59 enhance the pinocytosis and Phagocytosis activity of Raw-264.7, which imply Trim59 might mediate the cell-molecule interaction. Our results indicate Trim59 might be an essential accessory molecule in mediating BAM tumoricidal functions; and Trim59 is a phagocytosis-correlated molecule.
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Registered trials
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