• Proceedings of the Zoological Society Korea Conference
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• 2001.04a
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• pp.76-76
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• 2001

trithorax group ; SWI/SNF complex ; Mll ; Brm ; Brg1 ; Xenopus

• Proceedings of the Zoological Society Korea Conference
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• 2001.10a
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• pp.187.2-188
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• 2001

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1997.10b
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• pp.259.2-259
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• 1997

No Abstract, See Full Text

• International Journal of Oral Biology
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• v.31 no.3
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• pp.81-86
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• 2006

SET (Suppressor of variegation, Enhancer of zeste, and the Trithorax) domain-containing proteins are known to have methyltransferase activity at lysine residues of histone proteins. In this study, we identified a novel SET domain-containing protein from mouse and named Kodo7. Indeed, Kodo7 has methyltransferase activity at K9 residue of the H3 protein as demonstrated by a histone methyl-transferse activity assay using GST-tagged Kodo7. Confocal microscopy showed that Kodo7 is co-localized with histones in the nucleus. Interestingly, ectopic expression of Kodo7 by transient transfection induced cell death and treatment of the transfectants with a caspase-3 inhibitor, Ac-DEVD-AFC decreased Kodo7-induced apoptosis. These results suggest that Kodo7 induces apoptotic cell death through increased methylation of histones leading to transcriptional repression.

• Molecules and Cells
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• v.37 no.12
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• pp.841-850
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• 2014

Polycomb group (PcG) proteins are conserved chromatin regulators involved in the control of key developmental programs in eukaryotes. They collectively provide the transcriptional memory unique to each cell identity by maintaining transcriptional states of developmental genes. PcG proteins form multi-protein complexes, known as Polycomb repressive complex 1 (PRC1) and Polycomb repressive complex 2 (PRC2). PRC1 and PRC2 contribute to the stable gene silencing in part through catalyzing covalent histone modifications. Components of PRC1 and PRC2 are well conserved from plants to animals. PcG-mediated gene silencing has been extensively investigated in efforts to understand molecular mechanisms underlying developmental programs in eukaryotes. Here, we describe our current knowledge on PcG-mediated gene repression which dictates developmental programs by dynamic layers of regulatory activities, with an emphasis given to the model plant Arabidopsis thaliana.

• Development and Reproduction
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• v.15 no.4
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• pp.273-279
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• 2011

Epigenetic regulation is a phenomenon that changes the gene function without changing the underlying DNA sequences. Epigenetic status of chromosome is regulated by mechanisms such as histone modification, DNA modification, and RNAi silencing. In this review, we focused on histone methylation for epigenetic regulation in ES cells. Two antagonizing multiprotein complexes regulate methylation of histones to guide expression of genes in ES cells. The Polycomb repressive complex 2 (PRC2), including EED, EZH2, and SUZ12 as core factors, contributes to gene repression by increasing trimethylation of H3K27 (H3K27me3). In contrast, the Trithorax group (TrxG) complex including MLL is related to gene activation by making H3K4me3. PRC2 and TrxG accompany a variety of accessory proteins. Most prominent feature of epigenetic regulation in ES cells is a bivalent state in which H3K27me3 and H3K4me3 appear simultaneously. Concerted regulation of PRC2, TrxG complex, and H3K4- or H3K27-specific demethylases activate expression of pluripotency-related genes and suppress development-related genes in ES cells. Modified balance of the regulators also enables ES cells to efficiently differentiate to a variety of cells upon differentiating signals. More detailed insights on the epigenetic regulators and their action will lead us to better understanding and use of ES cells for future application.

• Journal of Gastric Cancer
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• v.17 no.4
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• pp.295-305
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• 2017

Purpose: We previously found that the histone methyltransferase suppressor of variegation, enhancer of zeste, trithorax and myeloid-nervy-deformed epidermal autoregulatory factor-1 domain-containing protein 3 (SMYD3) is a potential independent predictive factor or prognostic factor for overall survival in gastric cancer patients, but its roles seem to differ from those in other cancers. Therefore, in this study, the detailed functions of SMYD3 in cell proliferation and migration in gastric cancer were examined. Materials and Methods: SMYD3 was overexpressed or suppressed by transfection with an expression plasmid or siRNA, and a wound healing migration assay and Transwell assay were performed to detect the migration and invasion ability of gastric cancer cells. Additionally, an MTT assay and clonogenic assay were performed to evaluate cell proliferation, and a cell cycle analysis was performed by propidium iodide staining. Furthermore, the expression of genes implicated in the ataxia telangiectasia mutated (ATM) pathway and proteins involved in cell cycle regulation were detected by polymerase chain reaction and western blot analyses. Results: Compared with control cells, gastric cancer cells transfected with si-SMYD3 showed lower migration and invasion abilities (P<0.05), and the absence of SMYD3 halted cells in G2/M phase and activated the ATM pathway. Furthermore, the opposite patterns were observed when SMYD3 was elevated in normal gastric cells. Conclusions: To the best of our knowledge, this study provides the first evidence that the absence of SMYD3 could inhibit the migration, invasion, and proliferation of gastric cancer cells and halt cells in G2/M phase via the ATM-CHK2/p53-Cdc25C pathway. These findings indicated that SMYD3 plays crucial roles in the proliferation, migration, and invasion of gastric cancer cells and may be a useful therapeutic target in human gastric carcinomas.