• KSBB Journal
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• v.7 no.4
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• pp.302-307
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• 1992

Protein phosphatase 2A was obtained from a cytosolic fraction of bovine brain homogenate. The phosphatase activity using phosphorylated histone Hl as substrate was suppressed in the presence of liposomes composed of dipalmitoylphosphatidylcholine(DPPC) or the mixture of phosphatidylserine and DPPC. The binding of protein phosphatase to liposome was indicated by the facts that the phosphatase activity of the supernatant of protein phosphatase/multilayer vesicle mixture was decreased with increasing amount of liposome, and that [$^{125}I$]-labeled protein phosphatase was coeluted with liposome. However, the affinity of the protein for phospholipid membrane was not so high. On the other hand, okadaic acid and liposome reduced the phosphatase activity synergistically, which means that okadaic acid binds neither to lipid membrane nor to the membrane-associated phosphatase, The inhibitory effect of liposome was, therefore, ascribed to association of the protein phosphatase 2A with the lipid bilayer membrane.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.112.3-113
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• 2003

More than 30 isolates of Alternaria were obtained from various solanaceous crops in Korea. For all isolates, morphological characteristics of the conidia were determined and compared with those of representative isolates of A. solani and A. tomatophila. Pathogenicity test was performed to Potato, tomato, egg plant and red Pepper and molecular characteristics of them including the representative isolates were determined using sequence analyses of ITS rDNA and histone H3 gene, and URP-PCR analysis. Based on morphological characteristics, the isolates from the solanaceous crops were grouped as identical or very similar to either A. tomatophila(ATO), A. solani(ASO), and unidentified Altemaria sp.(ASP). Among the molecular markers used in this study, the URP-PCR analysis was found to be appropriate for taxonomic resolution of these species. Based on the conidial morphology, pathogenicity test and molecular characteristics, A. tomatophila(early blight of tomato) could be distinguished from A. solani(early blight of potato), and the Alternaria sp.(ASP) from potato, which was closely related to A. solani in conidial morphology, was considered as a new species.

• BMB Reports
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• v.53 no.2
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• pp.112-117
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• 2020

A recent study suggested that methylation of ubiquitin-like with PHD and RING finger domain 1 (UHRF1) is regulated by SET7 and lysine-specific histone demethylase 1A (LSD1) and is essential for homologous recombination (HR). The study demonstrated that SET7-mediated methylation of UHRF1 promotes polyubiquitination of proliferating cell nuclear antigen (PCNA), inducing HR. However, studies on mediators that interact with and recruit UHRF1 to damaged lesions are needed to elucidate the mechanism of UHRF1 methylation-induced HR. Here, we identified that poly [ADP-ribose] polymerase 1 (PARP1) interacts with damage-induced methylated UHRF1 specifically and mediates UHRF1 to induce HR progression. Furthermore, cooperation of UHRF1-PARP1 is essential for cell viability, suggesting the importance of the interaction of UHRF1-PARP1 for damage tolerance in response to damage. Our data revealed that PARP1 mediates the HR mechanism, which is regulated by UHRF1 methylation. The data also indicated the significant role of PARP1 as a mediator of UHRF1 methylation-correlated HR pathway.

• Natural Product Sciences
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• v.19 no.2
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• pp.127-136
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• 2013

Ionizing radiation, including that evoked by gamma (${\gamma}$)-rays, induces oxidative stress through the generation of reactive oxygen species, resulting in apoptosis, or programmed cell death. This study aimed to elucidate the radioprotective effects of hyperoside (quercetin-3-O-galactoside) against ${\gamma}$-ray radiation-induced apoptosis in Chinese hamster lung fibroblasts, V79-4 and demonstrated that the compound reduced levels of intracellular reactive oxygen species in ${\gamma}$-ray-irradiated cells. Hyperoside also protected irradiated cells against DNA damage (evidenced by pronounced DNA tails and elevated phospho-histone H2AX and 8-oxoguanine content) and membrane lipid peroxidation. Furthermore, hyperoside prevented the ${\gamma}$-ray-provoked reduction in cell viability via the inhibition of apoptosis through the increased levels of Bcl-2, the decreased levels of Bax and cytosolic cytochrome c, and the decrease of the active caspase 9 and caspase 3 expression. Taken together, these results suggest that hyperoside defend cells against ${\gamma}$-ray radiation-induced apoptosis by inhibiting oxidative stress.

• Biomolecules & Therapeutics
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• v.28 no.6
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• pp.519-526
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• 2020

Methamphetamine (MA) is one of the most commonly abused drugs in the world by illegal drug users. Addiction to MA is a serious public health problem and effective therapies do not exist to date. It has also been reported that behavior induced by psychostimulants such as MA is related to histone deacetylase (HDAC). MeBib is an HDAC6 inhibitor derived from a benzimidazole scaffold. Many benzimidazole-containing compounds exhibit a wide range of pharmacological activity. In this study, we investigated whether HDAC6 inhibitor MeBib modulates the behavioral response in MA self-administered rats. Our results demonstrated that the number of active lever presses in MA self-administered rats was reduced by pretreatment with MeBib. In the hippocampus of rats, we also found MA administration promotes GluN2B, an NMDA receptor subunit, expression, which results in sequential activation of ERK/CREB/BDNF pathway, however, MeBib abrogated it. Collectively, we suggest that MeBib prevents the MA seeking response induced by MA administration and therefore, represents a potent candidate as an MA addiction inhibitor.

• Journal of Microbiology and Biotechnology
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• v.30 no.6
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• pp.830-838
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• 2020

The histone-like nucleoid structuring protein (H-NS) is an abundant global regulator of environmentally controlled gene expression. Herein, we demonstrate that H-NS represses the expression of LeuO, the master regulator of the cyclic(Phe-Pro)-dependent signaling pathway, by directly binding to the upstream region of the gene. H-NS binds to a long stretched region (more than 160-bp long), which overlaps with binding sites for ToxR and LeuO. A high quantity of H-NS outcompetes ToxR for binding to the cis-acting element of leuO. However, our footprinting analyses suggests that the binding of H-NS is relatively weaker than LeuO or ToxR at the same molarity. Considering that the DNA nucleotide sequences of the upstream regions of leuO genes are highly conserved among various Vibrio, such patterns as those found in V. vulnificus would be a common feature in the regulation of leuO gene expression in Vibrionaceae. Taken together, these results suggest that, in species belonging to Vibrionaceae, H-NS regulates the expression of leuO as a basal stopper when cFP-ToxR mediated signaling is absent.

• Reproductive and Developmental Biology
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• v.38 no.1
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• pp.41-52
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• 2014

Embryonic genome activation (EGA) is a highly complex phenomenon that is controlled at various levels. New studies have ascertained some molecular mechanisms that control EGA in several species; it is apparent that these same mechanisms regulate EGA in all species. Protein phosphorylation, DNA methylation and histone modification regulate transcriptional activities, and mechanisms such as ubiquitination, SUMOylation and microRNAs post-transcriptionally regulate development. Each of these regulations is highly dynamic in the early embryo. A better understanding of these regulatory strategies can provide the possibility to improve the reproductive properties in mammals such as pigs, to develop methods of generating high-quality embryos in vitro, and to find markers for selecting developmentally competent embryos.

• Journal of Microbiology and Biotechnology
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• v.27 no.3
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• pp.610-615
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• 2017

When Shigella infect host cells, various effecter molecules are delivered into the cytoplasm of the host cell through the type III secretion system (TTSS) to facilitate their invasion process and control the host immune responses. Among these effectors, the S. flexneri effector OspF dephosphorylates mitogen-activated protein kinases and translocates itself to the nucleus, thus preventing histone H3 modification to regulate expression of proinflammatory cytokines. Despite the critical role of OspF, the mechanism by which it localizes in the nucleus has remained to be elucidated. In the present study, we identified a potential small ubiquitin-related modifier (SUMO) modification site within OspF and we demonstrated that Shigella TTSS effector OspF is conjugated with SUMO in the host cell and this modification mediates the nuclear translocation of OspF. Our results show a bacterial virulence factor can exploit host post-translational machinery to execute its intracellular trafficking.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1403-1410
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• 2014

Epigenetic regulators like histone deacetylases (1 and 2), and viral onco-proteins (E6/E7) are known to be overexpressed in cervical cancer cells. The present study was designed to investigate the effect of curcumin on HDACs (1 and 2) and HPV E6/E7 in the cervical cancer cell line SiHa and a drug resistant clone $SiHa^R$ (derived from SiHa). It was further intended to investigate whether curcumin could sensitize the cells towards cisplatin induced cell killing by modulation of multi drug resistant proteins like MRP1 and Pgp1. Curcumin inhibited HDACs, HPV expression and differentially increased acetylation and up-regulation of p53 in SiHa and $SiHa^R$, leading to cell cycle arrest at G1-S phase. Up-regulation of pRb, p21, p27 and corresponding inhibition of cyclin D1 and CDK4 were observed. Cisplatin resistance in $SiHa^R$ due to over-expression of MRP1 and Pgp1 was overcome by curcumin. Curcumin also sensitized both the cervical cancer cells towards cisplatin induced cell killing. Inhibition of HDACs and HPVs led to cell cycle arrest at G1/S phase by alteration of cell cycle regulatory proteins. Suppression of MRP1 and Pgp1 by curcumin resulted in sensitization of cervical cancer cells, lowering the chemotherapeutic dose of the drug cisplatin.

• Journal of Microbiology and Biotechnology
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• v.27 no.8
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• pp.1367-1378
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• 2017

Epigenetic alterations such as DNA methylation, histone acetylation, and chromatin remodeling can control gene expression by regulating gene transcription. DNA methylation is one of the frequent epigenetic events that play important roles in cancer development. Cancer cells can gain significant resistance to anticancer drugs and escape programmed cell death through major epigenetic changes, including DNA methylation. To date, several research groups have identified instances of both (i) hypermethylation of tumor suppressor genes, and (ii) global hypomethylation of oncogenes. These changes in DNA methylation status could be used as biomarkers for the diagnosis and prognosis of cancer patients undergoing chemotherapies or other clinical therapies. Herein, we describe genes for which methylation is dependent upon anticancer drug resistance in patients with gastric cancer; we then suggest a significant epigenetic target to focus on for overcoming anticancer drug resistance.