• Korean Journal of Microbiology
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• v.52 no.4
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• pp.487-494
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• 2016

In Saccharomyces cerevisiae, Paf1 complex consists of five proteins, and they are structurally and functionally well conserved in yeast, fruit fly, plants, and human. With binding to RNA polymerase II from transcription start site to termination site, Paf1 complex functions as a platform for recruiting many types of transcription factors to RNA polymerase II. Paf1 complex contributes to H2B ubiquitination and indirectly influences on H3K4 di- and tri-methylation by histone crosstalk. But the individual effects of five components in Paf1 complex on these two histone modifications including H2B ubiquitination and H3K4 methylation largely remained to be identified. In this study, we constructed the single-gene knockout mutants of each Paf1 complex component and observed H3K4 mono-, di-, and trimethylation as well as H2B ubiquitination in these mutants. Interestingly, in each ${\Delta}paf1$, ${\Delta}rtf1$, and ${\Delta}ctr9$ strain, we observed the dramatic defect in H3K4 monomethylation, which is independent of H2B ubiquitination, as well as H3K4 di- and trimethylation. However, the protein level of Set1, which is methyltransferase for H3K4, was not changed in these mutants. This suggests that Paf1 complex may directly influence on H3K4 methylation by directly regulating the activity of Set1 or the stability of Set1 complex in an H2B ubiquitination independent manner.

• Journal of Plant Biotechnology
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• v.38 no.1
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• pp.62-68
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• 2011

Calmodulin (CaM), a $Ca^{2+}$ binding protein in eukaryotes, mediates cellular $Ca^{2+}$ signals in response to a variety of biotic and abiotic external stimuli. The $Ca^{2+}$-bound CaM transduces signals by modulating the activities of numerous CaM-binding proteins. As a CaM binding protein, AtCBP63 ($\b{A}$rabidopsis thaliana $\b{C}$aM-binding protein $\underline{63}$ kD) has been known to be positively involved in plant defense signaling pathway. To investigate the pathogen resistance function of AtCBP63 in potato, we constructed transgenic potato (Solanum tuberosum L.) plants constitutively overexpressing AtCBP63 under the control of cauliflower mosaic virus (CaMV) 35S promoter. The overexpression of the AtCBP63 in potato plants resulted in the high level induction of pathogenesis-related (PR) genes such as PR-2, PR-3 and PR-5. In addition, the AtCBP63 transgenic potato showed significantly enhanced resistance against a pathogen causing bacterial soft rot, Erwinia carotovora ssp. Carotovora (ECC). These results suggest that a CaM binding protein from Arabidopsis, AtCBP63, plays a positive role in pathogen resistance in potato.

• Journal of Life Science
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• v.26 no.1
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• pp.8-16
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• 2016

Reactive oxygen species (ROS), at appropriate concentrations, mediate various normal cellular functions, including defense against pathogens, signal transduction, cellular growth, and gene expression. A recent study demonstrated that ROS and ROS-generating NADPH oxidase (Nox) are important in self-renewal and neuronal differentiation of subventricular zone (SVZ) neural stem cells in adult mouse brains. In this study, we found that endogenous ROS were detected in SVZ neural stem cells cultured from postnatal mouse brains. Nox4 was predominantly expressed in cultured cells, while the levels of the Nox1 and Nox2 transcripts were very low. In addition, the Nox4 gene was highly upregulated (by up to 10-fold) during neuronal differentiation. Immunocytochemical analysis detected the Nox4 protein mainly in neurons positive for the neuronal specific tubulin Tuj1. After differentiation, endogenous ROS were detected exclusively in neuron-like cells with processes. In addition, perturbation of the cellular redox state with N-acetyl cysteine, a ROS scavenger, during neuronal differentiation greatly inhibited neurogenesis. Lastly, knockdown of Nox4 using short hairpin RNA decreased neurogenesis. These findings suggest that Nox4 may be a major ROS-generating enzyme in postnatal SVZ neural stem cells, and Nox4-mediated ROS generation may be important in their neuronal differentiation.

• The Proceeding of the Korean Institute of Electromagnetic Engineering and Science
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• v.8 no.2
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• pp.37-55
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• 1997

최근 선진국가들에서는 전자파 장애 증후군에 관심이 집중되고 있는데, 전자파에 장기 노출 되는 인구에서 뇌암이나 유방암, 백혈병 등의 발생률이 높다는 보고(Kolmodin-Hedman 등, 1988 ; Demers등, 1991)가 있어서 전자제품의 생산업체는 물론이고 사용자에 대해서도 불안한 관심사가 되 어 있다. 전자파가 생체에 미치는 영향은 열적 효과와 비열적 효과에 의한 것으로 구분된다. Microwave는 약 300MHz에서 300GHz 사이(파장 1m에서 1mm사이)의 주파수를 가지는 전자파로서 이온의 운동이나 쌍극자분자(dipole molecule)들을 진동시키므로서 조직에 열이 발생한다. 열이 과도하게 발생하면 세포 단백질이 응고하게 되는 등 일반적으로 생각할 수 있는 고열로 인한 여러 가지 유해환경이 조직 에 조성될 수 있다. 실제로 고전압의 전자파에 노출된 안구의 수정체에 백내장 등의 병변이 발생한 것 으로 보고된 바 있다(Adey,1981). 일반적으로 전자파의 생체에 대한 작용으로는 이렇듯 조직에 흡수 되는 전자파의 에너지에 의한 열작용이 지배적인 것으로 생각되어 왔다. 그러나 초저주파역대(Extre- mely low frequency, EMF)의 변조 및 펄스파 등의 영향에 관해서도 조직의 온도상승으로는 설명할 수 없는 현상이 보고된 바 있다. 이러한 비열적 효과가 신경계에 끼치는 영향에 대해서는 혈액뇌관문 의 투과성 변화(Oscar와 Hawkins, 1977), 뇌종양 발생, 칼슘대사 이상 및 신경전달물질에 대한 영향 등이 주장(Anderson, 1993)되고 있으나 아직 그 분명한 기전이 밝혀져 있지 않은 상태이다. 또한 그 영향의 평가에 서도 일정한 기준이나 지표가 정해지지 않은 실정이다. 그러므로 신경계에 대한 대체적인 소개와 더불어 전자기파의 영향에 대한 이제까지의 보고를 종합 하고 향후 연구의 방향을 소개하고자 한다.> 이온이 공동 첨가제로 더 적합하다.u(30 .angs. )/CoFe(35 .angs. )/NiO(800 .angs. ) 구조를 갖는 spin-valve 박막은 극대 MR비 6.3%, 유효자기장감응도 약 0.5(%/Oe)를 보여 spin-valve head 재료로 적합함을 알 수 있었다.다.다.다.는 각각 148 meV .angs. $^{2}$, 103.8 meV .angs. $^{2}$와 1.77 * $10^{-6}$ erg/cm, 0.67 * $10^{-6}$ erg/cm 였다.다.자 노인들을 영주권자와 귀화 시민권자의 구분없이 하나의 집단으로 간주하고 분석해 왔던 것을 볼 때, 앞으로의 연구는 이론적으로나 방법론적으로 시민권의 유무가 주거형태에 끼치는 영향도 함께 고려해야 할 것이다.에 나타난 인도의 영향은 여성복식과 남성복식에 있어서 서로 유사점과 차이점이 보이는데, 인도의 영향이 여성복식에 있어서 그 빈도가 더 높고, 종류가 더 다양함을 볼 수 있다. 여성복식에 있어서는 12가지의 다양한 인도복식스타일이 나타났으며, 그중 가장 많이 보이는 스타일은 Indian Shirt/Blouse/Smock/ Dress이며, 그 뒤를 이어 Madras, Indian lowery등을 볼 수 있다. 남성복식애 나타난 7가지의 스타일 중에는 Madras가 가장 빈도가 높으며 그외의 스타일들은 그 빈도가 매우 낮음을 볼 수 있다. 인도의 영향의 정도 (Attribution Categories) 있어서는 여성과 남성복식 모두에 있어서 인도에서 직접 수입된(originated) item이 각각 전체의 90%와 81%를 차지하여, 인도복식의 영향은 받았으나 미국내에서 제작된(attributed and connotated) item 보다 휠씬 더 많은 수를 보였다. 인도복식스타일이 가장

• Journal of Life Science
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• v.26 no.10
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• pp.1182-1188
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• 2016

Membrane-associated guanylate kinase inverted-3 (MAGI-3) is a member of the family of membrane-associated guanylate kinases (MAGUKs). MAGI-3 modulates the kinase activity of protein kinase B (PKB)/AKT through interactions with phosphatase and tensin homolog (PTEN)/MMAC. Coxsackievirus B3 (CVB3) is a common causative agent of acute myocarditis and chronic dilated cardiomyopathy. Activation of AKT and extracellular signal-regulated kinases 1/2 (ERK1/2) is essential for CVB3 replication, but the relation between MAGI-3 signaling and CVB3 replication is not well understood. This study investigated the role of MAGI-3 in CVB3 infection and replication. MAGI-3 was overexpressed in HeLa cells by polyethylenimine (PEI) transfection. To optimize the transfection conditions, different ratios of plasmid DNA to PEI concentrations were used. MAGI-3 and empty plasmid DNA were transfected into the HeLa cells. MAGI-3 overexpression alone was not sufficient to efficiently activate AKT. However, expression of the CVB3 capsid protein VP1 dramatically increased in the HeLa cells overexpressing MAGI-3 24 h after CVB3 infection. In addition, the activities of AKT and ERK were significantly induced in the CVB3-infected MAGI-3 cells overexpressing HeLa. These results demonstrate that MAGI-3 expression upregulates CVB3 replication through AKT and ERK signaling activation. MAGI-3 may be an important target to control CVB3 replication.

• Journal of Life Science
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• v.28 no.10
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• pp.1233-1243
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• 2018

Sterol regulatory-element binding proteins (SREBPs) are a family of transcription factors that regulate lipid homeostasis and metabolism by controlling the expression of enzymes required for endogenous cholesterol, fatty acid (FA), triacylglycerol, and phospholipid synthesis. The three SREBPs are encoded by two different genes. The SREBP1 gene gives rise to SREBP-1a and SREBP-1c, which are derived from utilization of alternate promoters that yield transcripts in which distinct first exons are spliced to a common second exon. SREBP-2 is derived from a separate gene. Additionally, SREBPs are implicated in numerous pathogenic processes, such as endoplasmic reticulum stress, inflammation, autophagy, and apoptosis. They also contribute to obesity, dyslipidemia, diabetes mellitus, and nonalcoholic fatty liver diseases. Genome-wide analyses have revealed that these versatile transcription factors act as important nodes of biological signaling networks. Changes in cell metabolism and growth are reciprocally linked through SREBPs. Anabolic and growth signaling pathways branch off and connect to multiple steps of SREBP activation and form complex regulatory networks. SREBPs are activated through the PI3K-Akt-mTOR pathway in these processes, but the molecular mechanism remains to be understood. This review aims to provide a comprehensive understanding of the role of SREBPs in physiology and pathophysiology at the cell, organ, and organism levels.

• Journal of Ginseng Research
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• v.24 no.4
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• pp.168-175
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• 2000

Relatively little is known about the signaling mechanism of ginseng saponins (ginsenosides), active ingredients of ginseng, in non-neuronal cells. Here, we describe that ginsenosides utilize a common pathway of receptor-mediated signaling pathway in Xenopus oocytes: increase in intracellular $Ca^{2+}$ concentration via phospholipase C (PLC) and $Ca^{2+}$ mobilization. Ginsenosides induced a marked and robust artivation of $Ca^{2+}$-activated Cl- channels in Xenopus oocytes. The effect of ginsenosides was completely reversible, in a dose-dependent manner with EC$_{50}$ of 4.4 $\mu\textrm{g}$/mi, and specifically blocked by niflumic acid, an inhibitor of $Ca^{2+}$-activated Cl- channel. Intracellular injection of BAPIA abolished the effect of ginsenosides. Intracellular injection of GTP${\gamma}$S also abolished the effect of ginsenosides. The effect of gin senosides on $Ca^{2+}$-activated Cl- currents was greatly reduced by the intracellular injection of heparin, an IP$_3$ receptorantagonist or the pretreatment of PLC inhibitor. These results indicate that ginsenosides activate endogenous $Ca^{2+}$-activated Cl- channels via the activation of PLC and the release of $Ca^{2+}$ from the IP$_3$-sensitive intracellular store following the initial interaction with membrane component(s) from extracellular side. This signaling pathway of ginsenosides may be one of the action mechanisms for the pharmacological effects of ginseng.ts of ginseng.

• KSBB Journal
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• v.20 no.1 s.90
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• pp.21-25
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• 2005

Paraquat, a widely used herbicide, has been suggested as a potential risk factor for Parkinson's disease. Heme oxygenase-1(HO-1), a marker for oxidative stress and endoplasmic reticulum(ER) stress, is known to catalyze heme to biliverdin, carbon monoxide and free iron in response to various stimuli. Here we show that paraquat activates HO-1 expression in a time-and dose-dependent manner in substantia nigra(SN) dopaminergic neuronal cells. Activation of Ho-1 by paraquat was regulated primarily at the level of gene transcription. Deletion analysis of the promoter and the 5' distal enhancers, E1 and E2, of the HO-1 gene revealed that the E2 enhancer is a potent inducer of the paraquat-dependent Ho-1 gene expression in dopamninergic neuronal cells. Mutational analysis of the E2 enhacer further demonstrated that the transcription factor activator protein-1(AP-1) plays an important role in mediating paraquat-induced HO-1 gene transcription. Moreover, using specific inhibitors of the mitogen-activated protein kinases(MAPKs), we investigated the role of paraquat and MAPKs for HO-1 gene regulation in dopaminergic cells. The c-Jun N-terminal kinase(JNK) inhibitor SP600125 significantly suppressed the expression of HO-1 by paraquat. All these results demonstrate that induction of HO-1 by paraquat requies the activation of the AP-1 and JNK pathway.

• Journal of Life Science
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• v.16 no.1
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• pp.30-36
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• 2006

Neutrophils are short-lived leukocytes that play a vital role in immune responses to bacteria, yeast, and fungi. This study was performed to investigate the effect of 4-O-methyl-ascochlorin (MAC), an anti-tumor, antibiotic, and anti-fungal prenyl-phenol compound on the spontaneous apoptosis of human neutrophils. MAC time- and dose-dependently accelerated the spontaneous apoptosis of human neutrophils. The effect of MAC on neutrophil apoptosis was blocked by pre-treatment of the neutrophils with specific inhibitors of pancaspase (zVAD-fmk), caspase-8 (zIETD-fmk), or caspase-3 (zDEVD-fmk). The cleavage of procaspase-8 and procaspase-3 was increased by MAC. Mitochondrial permeability, which was measured by the retention of $DiOC_6(3)$, was dose-de-pendently increased by MAC but the change of mitochondrial permeability was not blocked by pretreatment of neutrophils with zIETD-fmk. These results suggest that MAC induces neutrophil apoptosis by caspase-8-dependent but mitochondria-independent manner.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.17 no.1
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• pp.152-158
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• 2016

Glutamate is one of the major excitatory neurotransmitters in the central nervous system of vertebrates. Human GDH (hGDH) is the enzyme that regulates the glutamate metabolism and its expression is higher in the brains of schizophrenia patients than in normal subjects. This study examined the changes in the hGDH enzymatic activity caused by antipsychotic drugs (haloperidol, risperidone, (${\pm}$)-sulpride, chlopromazine hydrochloride, melperone, (${\pm}$)butaclamol, domperidone, clozapine) related to schizophrenia. First of all, hGDH isozymes (hGDH1, hGDH2) were synthesized by genetic recombination. As a result of the enzyme assay, haloperidol, (${\pm}$)-sulpride, melperone and clozapine had an inhibitory effect on the hGDH isozymes. In addition, haloperidol showed a non-competitive inhibition against the substrate, 2-oxoglutarate. In contrast, it showed an uncompetitive inhibition against another substrate, NADH. The inhibitory effect of haloperidol on hGDH2 was abolished by the presence of L-leucine, an allosteric effector of hGDH, but by not other antipsychotic drugs. These results revealed the inhibition of enzyme activity by psychotropic drugs in hGDH isoenzymes (hGDH1 and hGDH2) and the possibility that haloperidol may be used to regulate the GDH activity and glutamate concentration in the central nervous system.