• Korean Journal of Veterinary Research
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• v.52 no.2
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• pp.99-104
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• 2012

The present study was performed to evaluate the relationship between the neurotoxicity of acrylamide and the differential gene expression pattern in mice. Both locomotor test and rota-rod test showed that the group treated with higher than 30 mg/kg/day of acrylamide caused impaired motor activity in mice. Based on cDNA microarray analysis of mouse brain, myelin basic protein gene, kinesin family member 5B gene, and fibroblast growth factor (FGF) 1 and its receptor genes were down-regulated by acrylamide. The genes are known to be essential for neurofilament synthesis, axonal transport, and neuroprotection, respectively. Interestingly, both FGF 1 and its receptor genes were down-regulated. Genes involved in nucleic acid binding such as AU RNA binding protein/enoyl-coA hydratase, translation initiation factor (TIF) 2 alpha kinase 4, activating transcription factor 2, and U2AF 1 related sequence 1 genes were down-regulated. More interesting finding was that genes of both catalytic and regulatory subunit of protein phosphatases which are important for signal transduction pathways were down-regulated. Here, we propose that acrylamide induces neurotoxicity by regulation of genes associated with neurofilament synthesis, axonal transport, neuro-protection, and signal transduction pathways.

• Reproductive and Developmental Biology
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• v.39 no.4
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• pp.97-104
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• 2015

Glucose is universal and essential fuel of energy metabolism and in the synthesis pathways of all mammalian cells. Glucose is the one of the major precursors of lactose synthesis using glycolysis result in producing milk fat and protein. During the milk fat synthesis, lipoprotein lipase (LPL) and CD36 are required for glucose uptake. Various morecules such as acyl-CoA synthetase 1 (ACSL1) activity of acetyl-CoA synthetase 2 (ACSS2), ACACA, FASN AGPAT6, GPAM, LPIN1 are closely related with milk fat synthesis. Additionally, glucose plays a major role for synthesizing lactose. Activations of lactose synthesize enzymes such as membranebound enzyme, beta-1,4-galactosyl transferase (B4GALT), glucose-6-phosphate dehydrogenase (G6PD) are changed by concentration of glucose in blood resulting change of amount of lactose production. Glucose transporters are a wide group of membrane proteins that facilitate the transport of glucose over a plasma membrane. There are 2 types of glucose transporters which consisted facilitative glucose transporters (GLUT); and sodium-dependent transport, mediated by the Na+/glucose cotransporters (SGLT). Among them, GLUT1, GLUT8, GLUT12, SGLT1, SGLT2 are main glucose transporters which involved in mammary gland development and milk synthesis. However, more studies are required for revealing clear mechanism and function of other unknown genes and transporters. Therefore, understanding of the mechanisms of glucose usage and its regulation in mammary gland is very essential for enhancing the glucose utilization in the mammary gland and improving dairy productivity and efficiency.

• Proceedings of the KSAR Conference
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• 2004.06a
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• pp.230-230
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• 2004

Polyamines, namely putrescine, spermidine, and spermine, are biogenic low-molecular-weight aliphatic amines. Polyamines play important roles in DNA stabilization, RNA and protein synthesis, membrane stabilization, modulation of ion channels, and protection against oxygen radicals and are essential for cell homeostasis, cell growth, and tumorigenesis. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.4
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• pp.287-291
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• 2012

This study investigated the effects of proline-serine (PS) and valine-serine (VS) dipeptides on melanogenesis in Mel-Ab cells. Proline-serine and VS significantly inhibited melanin synthesis in a concentration-dependent manner, though neither dipeptide directly inhibited tyrosinase activity in a cell-free system. Both PS and VS down-regulated the expression of microphthalmia-associated transcription factor (MITF) and tyrosinase. In a follow-up study also described here, the effects of these dipeptides on melanogenesis-related signal transduction were quantified. Specifically, PS and VS induced ERK phosphorylation, though they had no effect on phosphorylation of the cAMP response element binding protein (CREB). These data suggest that PS and VS inhibit melanogenesis through ERK phosphorylation and subsequent down-regulation of MITF and tyrosinase. Properties of these dipeptides are compatible with application as skin-whitening agents.

• Journal of Periodontal and Implant Science
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• v.34 no.2
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• pp.345-356
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• 2004

The triclosan was shown to have anti-microbial and anti-inflammatory effect with inhibition of inflammatory mediators such as prostaglandin $E_2(PGE_2)$. The purpose of this study was to elucidate whether and how $PGE_2$ could be inhibited by triclosan in human gingival fibroblast. Human gingival fibroblast-1 cells (ATCC CRL2014) were pre-treated for 1 hour with triclosan (0.001 ${\mu}/ml{\sim}10$ ${\mu}/ml$) and then stimulated with $TNF-{\alpha}$ (1.0 ng/ml). $PGE_2$ synthesis was evaluated by ELISA and gene expression of COX-1 and COX-2 was evaluated by RT-PCR after $TNF-{\alpha}$, triclosan, and NS-398 (COX-2 inhibitor, 5, ${\mu}M$) and/ or cycloheximide (protein synthesis inhibitor, 2 ${\mu}g/ml$). Triclosan was cytotoxic to human gingival fibroblasts in the concentration higher than 1.0 ${\mu}g/ml$ for longer than 24 hours in tissue culture. The $PGE_2$ synthesis was inhibited by triclosan in dose-dependent manner. Greater COX-2 mRNA suppression was observed with triclosan (0.1 ${\mu}g/ml$) than with $TNF-{\alpha}$ alone, without change in COX-1 gene expression. Inhibitory effects of triclosan on $PGE_2$ synthesis disappeared in presence of cycloheximide. This study suggests that triclosan inhibit prostaglandin $E_2$ at the level of COX-2 gene regulation and require de novo protein synthesis.

• Journal of Microbiology
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• v.39 no.1
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• pp.42-48
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• 2001

The regulation of actin gene expression during the differentiation of Naegleria gruberi was examined. Actin mRNA concentration was maximal in amoebae and decreased rapidly after the initiation of differentiation. At 20 min after initiation, the concentration of actin mRNA decreased to 55% of the maximal value. The actin mRNA concentration decreased to the minimum at 80 min (15% of the maximum), and then began to increase slightly at the end of differentiation. This decrease of actin mRNA concentration was regulated by the repression of actin gene transcription based on nuclear run-on transcription experiments. The rates of transcription of actin gene in nuclei prepared at 40 and 80 min after the initiation of differentiation were 50 and 28% of that of nuclei prepared at the beginning of differentiation, respectively. The addition of cycloheximide at the initiation of differentiation inhibited both the rapid decrease in the concentration of actin mRNA and the repression of actin gene transcription. These results suggest that the rapid decrease in the concentration of actin mRNA during the differentiation of N. gruberi is accomplished by the repression of actin gene transcription and this transcriptional regulation requires continuous protein synthesis during the differentiation.

• Animal Bioscience
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• v.37 no.3
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• pp.509-521
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• 2024

Objective: It was shown that microRNAs (miRNAs) play an important role in milk protein synthesis. However, the post-transcriptional regulation of casein expression by exogenous miRNA (xeno-miRNAs) in ruminants remains unclear. This study explores the regulatory roles of alfalfa xeno-miR162 on casein synthesis in bovine mammary epithelial cells (bMECs). Methods: The effects of alfalfa xenomiR-162 and G protein subunit gamma 11 (GNG11) on proliferation and milk protein metabolism of bMECs were detected by 5-Ethynyl-2'-Deoxyuridine (EdU) staining, flow cytometry, cell counting kit-8 (CCK-8), enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. Dual-luciferase reporter assay was used to verify the targeting relationship between GNG11 and xenomiR-162. Results: Results showed that over-expression of xenomiR-162 inhibited cell proliferation but promoted apoptosis, which also up-regulated the expression of several casein coding genes, including CSN1S1, CSN1S2, and CSN3, while decreasing the expression of CSN2. Furthermore, the targeting relationship between GNG11 and xenomiR-162 was determined, and it was confirmed that GNG11 silencing also inhibited cell proliferation but promoted apoptosis and reduced the expression of casein coding genes and genes related to the mammalian target of rapamycin (mTOR) pathway. Conclusion: Alfalfa xenomiR-162 appears to regulate bMECs proliferation and milk protein synthesis via GNG11 in the mTOR pathway, suggesting that this xeno-miRNA could be harnessed to modulate CSN3 expression in dairy cows, and increase κ-casein contents in milk.

• BMB Reports
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• v.34 no.4
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• pp.379-384
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• 2001

The cDNA encoding ribosomal protein was identified from a cDNA library of Schizosaccharomyces pombe. The nucleotide sequence of the 548 by cDNA clone reveals an open reading frame, which encodes a putative protein of 166 amino acids with a molecular mass of 18.3 kDa. The amino acid sequence of the S. pombe L11 protein is highly homologous with those of rat and fruit, while it is clearly less similar to those of prokaryotic counterparts. The 1,044 by upstream sequence, and the region encoding N-terminal 7 amino acids of the genomic DNA were fused into the promoterless $\beta$-galactosidase gene of the shuttle vector YEp357 in order to generate the fusion plasmid pHY L11. Synthesis of $\beta$-galactosidase from the fusion plasmid varied according to the growth curve. It decreased significantly in the growth-arrested yeast cells that were treated with aluminum chloride and mercuric chloride. However, it was enhanced by treatments with cadmium chloride ($2.5\;{\mu}M$), zinc chloride ($2.5\;{\mu}M$), and hydrogen peroxide (0.5 mM). This indicates that the expression of the L,11 gene could be induced by oxidative stress.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.70-70
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• 2003

Estrogen receptor is a ligand-activated transcription factor. Its action depends on the receptor, its ligand, and its coactivator proteins. As a consequence, the concentration of the receptor is a major component that governs the magnitude of the estrogen response. Despite the extensive knowledge on mechanism of estrogen receptor action, regulation of estrogen receptor itself is not very well understood. Estrogen receptor is known to be downregulated under hypoxia leading to inhibition of estrogen receptor mediated transcription activation. We have studied mechanism of loss of estrogen responsiveness under hypoxia. We found that Hif-l${\alpha}$, a major transcription factor regulating hypoxic response, inhibited transcription of estrogen response element driven luciferase gene by expression of HIF-l${\alpha}$/vp16 construct designed to contain transcription activity under normoxia. This loss of estrogen responsiveness appears to be the result of ER${\alpha}$ downregulation. ER${\alpha}$was downregulated at the levels of ligand-biding and protein within l2-24h, and the response was blocked by the proteasome inhibitor MG132, protein synthesis inhibitor cyclohexamide, and tyrosine kinase inhibitor Genistein. These results demonstrate that Hif-l${\alpha}$ downregulates ER${\alpha}$ by proteasome dependent pathway.

• Journal of Marine Bioscience and Biotechnology
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• v.1 no.4
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• pp.243-251
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• 2006

Dideoxypetrosynol A, a polyacetylene from the marine sponge Petrosia sp., is known to exhibit significant selective cytotoxic activity against a small panel of human tumor cell lines, however, the mechanisms of which are poorly understood. In the present study, it was investigated the further possible mechanisms by which dideoxytetrosynol A exerts its anti-proliferative action in cultured human leukemia cell line U937. We observed that the proliferation-inhibitory effect of dideoxypetrosynol A was due to the induction of G1 arrest of the cell cycle and apoptosis, which effects were associated with up-regulation of cyclin D1 and down-regulation of cyclin E without any change in cyclin-dependent-kinases (Cdks) expression. Dideoxypetrosynol A markedly induced the levels of Cdk inhibitor p16/INK4a expression. Furthermore, down-regulation of phosphorylation of retinoblastoma protein (pRB) by this compound was associated with enhanced binding of pRB and the transcription factor E2F-1. The increase in apoptosis was associated with a dose-dependent up-regulation in pro-apoptotic Bax expression and activation of caspase-3 and caspase-9. Dideoxytetrosynol A decreased the levels of cyclooxygenase (COX)-2 mRNA and protein expression without significant changes in the levels of COX-1, which was correlated with a decrease in prostaglandin E2 (PGE2) synthesis. Furthermore, dideoxytetrosynol A treatment markedly inhibited the activity of telomerase, and the expression of human telomerase reverse transcriptase (hTERT), a main determinant of the telomerase enzymatic activity, was progressively down-regulated by dideoxytetrosynol A treatment in a dose-dependent fashion. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of dideoxytetrosynol A.