• Proceedings of the PSK Conference
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• 2003.04a
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• pp.229.1-229.1
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• 2003

The anti proliferative effects of bile acids and their derivatives on HT -29 human colon cancer cells were investigated. Ursodeoxycholic acid (UDCA) and its synthetic derivatives, HS-1030 and HS-1183, and chenodeoxycholic acid (CDCA) and its synthetic derivatives, HS-1199 and HS-1200 were employed for this study. General evaluations focusing on cell cycle were conducted in HT -29 human colon adenocarcinoma cell line (p53 mutant type). (omitted)

• Journal of Microbiology and Biotechnology
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• v.23 no.10
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• pp.1381-1385
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• 2013

The centipede Scolopendra subpinipes mutilans is a medicinally important arthropod species. However, its transcriptome is not currently available and transcriptome analysis would be useful in providing insight into a molecular level approach. Hence, we performed de novo RNA sequencing of S. subpinipes mutilans using next-generation sequencing. We generated a novel peptide (scolopendrasin II) based on a SVM algorithm, and biochemically evaluated the in vitro antimicrobial activity of scolopendrasin II against various microbes. Scolopendrasin II showed antibacterial activities against gram-positive and -negative bacterial strains, including the yeast Candida albicans and antibiotic-resistant gram-negative bacteria, as determined by a radial diffusion assay and colony count assay without hemolytic activity. In addition, we confirmed that scolopendrasin II bound to the surface of bacteria through a specific interaction with lipoteichoic acid and a lipopolysaccharide, which was one of the bacterial cell-wall components. In conclusion, our results suggest that scolopendrasin II may be useful for developing peptide antibiotics.

• BMB Reports
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• v.49 no.2
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• pp.99-104
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• 2016

The nuclear non-histone protein high mobility group box (HMGB) 1 is known to having an inhibitory effect on the repair of DNA damaged by the antitumor drug cisplatin in vitro. To investigate the role of HMGB1 in living cells, we studied the DNA repair of cisplatin damages in mouse fibroblast cell line, NIH-3T3. We evaluated the effect of the post-synthetic acetylation and C-terminal domain of the protein by overexpression of the parental and mutant GFP fused forms of HMGB1. The results revealed that HMGB1 had also an inhibitory effect on the repair of cisplatin damaged DNA in vivo. The silencing of HMGB1 in NIH-3T3 cells increased the cellular DNA repair potential. The increased levels of repair synthesis could be "rescued" and returned to less than normal levels if the knockdown cells were transfected with plasmids encoding HMGB1 and HMGB1 K2A. In this case, the truncated form of HMGB1 also exhibited a slight inhibitory effect.

• Molecules and Cells
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• v.38 no.12
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• pp.1105-1110
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• 2015

Phleichrome, a pigment produced by the phytopathogenic fungus Cladosporium phlei, is a fungal perylenequinone whose photodynamic activity has been studied intensively. To determine the biological function of phleichrome and to engineer a strain with enhanced production of phleichrome, we identified the gene responsible for the synthesis of phleichrome. Structural comparison of phleichrome with other fungal perylenequinones suggested that phleichrome is synthesized via polyketide pathway. We recently identified four different polyketide synthase (PKS) genes encompassing three major clades of fungal PKSs that differ with respect to reducing conditions for the polyketide product. Based on in silico analysis of cloned genes, we hypothesized that the non-reducing PKS gene, Cppks1, is involved in phleichrome biosynthesis. Increased accumulation of Cppks1 transcript was observed in response to supplementation with the application of synthetic inducer cyclo-(${_L}-Pro-{_L}-Phe$). In addition, heterologous expression of the Cppks1 gene in Cryphonectria parasitica resulted in the production of phleichrome. These results provide convincing evidence that the Cppks1 gene is responsible for the biosynthesis of phleichrome.

• Molecules and Cells
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• v.40 no.8
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• pp.577-586
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• 2017

Phytocystatins (PhyCYSs) are plant-specific proteinaceous inhibitors that are implicated in protein turnover and stress responses. Here, we characterized a PhyCYS from Arabidopsis thaliana, which was designated AtCYS5. RT-qPCR analysis showed that the expression of AtCYS5 in germinating seeds was induced by heat stress (HS) and exogenous abscisic acid (ABA) treatment. Analysis of the expression of the ${\beta}-glucuronidase$ reporter gene under the control of the AtCYS5 promoter showed that AtCYS5 expression during seed germination was induced by HS and ABA. Constitutive overexpression of AtCYS5 driven by the cauliflower mosaic virus 35S promoter led to enhanced HS tolerance in transgenic Arabidopsis, which was characterized by higher fresh weight and root length compared to wild-type (WT) and knockout (cys5) plants grown under HS conditions. The HS tolerance of AtCYS5-overexpressing transgenic plants was associated with increased insensitivity to exogenous ABA during both seed germination and post-germination compared to WT and cys5. Although no HS elements were identified in the 5'-flanking region of AtCYS5, canonical ABA-responsive elements (ABREs) were detected. AtCYS5 was upregulated in ABAtreated protoplasts transiently co-expressing this gene and genes encoding bZIP ABRE-binding factors (ABFs and AREB3). In the absence of ABA, ABF1 and ABF3 directly bound to the ABREs in the AtCYS5 promoter, which activated the transcription of this gene in the presence of ABA. These results suggest that an ABA-dependent pathway plays a positive role in the HS-responsive expression of AtCYS5 during seed germination and post-germination growth.

• Korean Journal of Agricultural Science
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• v.45 no.2
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• pp.185-196
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• 2018

The fungus gnat, Bradysia difformis, damages various crops in greenhouses and is recognized as an important pest around the world. Additionally, in the future, many other greenhouse crops will be added to the list of crops damaged by the fungus gnat. In this study, to find effective control methods for the fungus gnat, the insecticidal effect of 20 chemical synthetic insecticides was tested with the potato disc and pot treatment methods; additionally, the control effect of 16 strains of B. thuringiensis was examined with the potato disk method. The fungus gnat larvae were treated for 2 days with each of the synthetic insecticides to determine insecticidal effect using the potato disc method. The results were as follows. Among the highly insecticidal active pesticides, chlorfenapyr exhibited a 100% insecticidal activity, and fenazaquin, acetamiprid, dinotefuran, fenthion and thiamethoxam exhibited more than a 90% insecticidal activity. For the pot treatment method, chlorfenapyr exhibited a 3.3% insecticidal effect, and thiamethoxam, acetamiprid, dinotefuran, fenthion, etc. exhibited an insecticidal effect of less than 10% of the emergence rate to adult fungus gnat after 14 days of treatment. To select the B. thuringiensis strains that have an insecticidal effect on the fungus gnat, 16 strains were biologically assayed using the potato disc method. Among the 16 strains, Bt-3, Bt-8 and Bt-13 had more than a 70% insecticidal effect. The $LC_{50}$ and $LC_{95}$ values of Bt-3, Bt-8 and Bt-13 were $3.7{\times}10^5$ and $4.7{\times}10^8cfu/ml$, $1.4{\times}10^5$ and $1.1{\times}10^7cfu/ml$, and $1.4{\times}10^5$ and $1.3{\times}10^7cfu/ml$, respectively.

• Journal of Plant Biology
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• v.34 no.4
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• pp.325-330
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• 1991

The ability of several auxin analogs to induce ethylene production was tested in the corn coleoptile. The synthetic auxins 1-naphthaleneacetic acid (1-NAA) and 2, 4-dichlorophenoxyacetic acid (2, 4-D) had strong stimulatory effects on ethylene induction surpassing that of IAA. Both 2-naphthalaneacetic acid (2-NAA) and 2, 6-dichlorophenoxy acetic acid (2, 6-D), structural analogs of these auxins, respectively, were found to be inactive. Treatment with NPA, a strong inhibitor of polar auxin transport, led to drastic increase in IAA-induced ethylene production while it has bo effect on ethylene production induced by 1-NAA. A positive correlative existed between intracellular auxin level and ethylene production.

• Proceedings of the Zoological Society Korea Conference
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• 2000.10a
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• pp.245.2-246
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• 2000

No Abstract, See Full Text

• The Korean Journal of Zoology
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• v.37 no.4
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• pp.488-494
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• 1994

Apolipophorin-III (ApoLp-III) was purified from adult haemolynph of Hyphantriu cuneo and their molecular weight and synthetic place were investigated. ApoLp-III purification was performed by KBr-density gradient ultracentrifugation followed by gel permeation chromatographv (Sephadex G-1001 and ion-exchange chromatography (CM-52) and their purity was confirmed on 10% SDS-PAGE. ApoLp-III has the molecular weight of 18 ItDa and is synthesized by fat body.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.5
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• pp.253-257
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• 2004

Schwann cells play an important role in peripheral nerve regeneration. Upon neuronal injury, activated Schwann cells clean up the myelin debris by phagocytosis, and promote neuronal survival and axon outgrowth by secreting various neurotrophic factors. However, it is unclear how the nerve injury induces Schwann cell activation. Recently, it was reported that certain cytoplasmic molecules, which are secreted by cells undergoing necrotic cell death, induce immune cell activation via the toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve damage by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. Accordingly, this study was undertaken to examine the expression and the function of the TLRs on primary Schwann cells and iSC, a rat Schwann cell line. The transcripts of TLR2, 3, 4, and 9 were detected on the primary Schwann cells as well as on iSC. The stimulation of iSC with poly (I : C), a synthetic ligand for the TLR3, induced the expression of $TNF-{\alpha}$ and RANTES. In addition, poly (I : C) stimulation induced the iNOS expression and nitric oxide secretion in iSC. These results suggest that the TLRs may be involved in the inflammatory activation of Schwann cells, which is observed during Wallerian degeneration after a peripheral nerve injury.