• Title/Summary/Keyword: defense proteins

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Future Prospects for Industrial Application of Abscisic acid, a Stress-resistant Phytohormone (스트레스 내성 식물 호르몬인 앱시스산의 산업적 활용 전망)

  • Lee, Jeongho;Kim, Seunghee;Yoo, Hah Young
    • Korean Chemical Engineering Research
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    • v.58 no.4
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    • pp.514-523
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    • 2020
  • Plants are exposed to various types of stresses in their surroundings, and stress-resistant and regulatory proteins are produced as defense mechanisms. Abscisic acid is well known for its important role in stress signals as a phytohormone and is also involved in the physiological reactions of plants such as leaf senescence and seed dormancy. In particular, it has been found to perform a variety of functions in other biological systems, such as animals and microalgae, not plants. In this review, the biosynthesis and signaling process of abscisic acid and its function were investigated and the future prospects for the industrial application of abscisic acid in various biotechnologies, including agriculture, biomedical and industrial biotechnology, have been proposed based on study of emerging applications such as increased crop yields, disease treatment development and bioenergy production.

Enhancement of Spermidine Content and Antioxidant Capacity by Modulating Ginseng Spermidine synthase in Response to Abiotic and Biotic Stresses

  • Parvin, Shohana;Lee, Ok-Ran;Sathiyaraj, Gayathri;Kim, Yu-Jin;Khorolragchaa, Altanzul;Yang, Deok-Chun
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2011.10a
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    • pp.14-14
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    • 2011
  • Polyamines (putrescine, spermidine and spermine) play pivotal roles in plant defense to different abiotic and biotic stresses. In order to understand the function of ginseng spermidine synthase gene, a key gene involved in biosynthesis of polyamines, transgenic plant was generated in Arabidopsis. The transgenic plants exhibited high levels of polyamines compared to the untransformed control plants. We investigated the tolerance capacity of transgenic plants to abiotic stresses such as salinity and copper stress. In addition, transgenic plants also showed increased resistance against one of the important fungal pathogens of ginseng, the wilt causing Fusarium oxysporum and one of important bacteria, bacterial blight causing Pseudomonas syringae. However, an activity of the polyamine catabolic enzyme, diamine oxidase (DAO) was increased significantly in F. oxysporum and P. syringae infected transgenic plant. Polyamine catabolic enzymes which may trigger the hypersensitive response (HR) by producing hydrogen peroxide ($H_2O_2$) seem act as an inducer of PR proteins, peroxidase and phenyl ammonium lyase activity. The transgenic plants also contained higher antioxidant enzyme activities, less MDA and $H_2O_2$ under salt and copper stress than the wild type, implying it suffered from less injury. These results strongly suggest an important role of spermidine as a signaling regulator in stress signaling pathways, leading to build-up of stress tolerance mechanisms.

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Activation of JNK and c-Jun Is Involved in Glucose Oxidase-Mediated Cell Death of Human Lymphoma Cells

  • Son, Young-Ok;Jang, Yong-Suk;Shi, Xianglin;Lee, Jeong-Chae
    • Molecules and Cells
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    • v.28 no.6
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    • pp.545-551
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    • 2009
  • Mitogen-activated protein kinases (MAPK) affect the activation of activator protein-1 (AP-1), which plays an important role in regulating a range of cellular processes. However, the roles of these signaling factors on hydrogen peroxide ($H_2O_2$)-induced cell death are unclear. This study examined the effects of $H_2O_2$ on the activation of MAPK and AP-1 by exposing the cells to $H_2O_2$ generated by either glucose oxidase or a bolus addition. Exposing BJAB or Jurkat cells to $H_2O_2$ affected the activities of MAPK differently according to the method of $H_2O_2$ exposure. $H_2O_2$ increased the AP-1-DNA binding activity in these cells, where continuously generated $H_2O_2$ led to an increase in mainly the c-Fos, FosB and c-Jun proteins. The c-Jun-$NH_2$-terminal kinase (JNK)-mediated activation of c-Jun was shown to be related to the $H_2O_2$-induced cell death. However, the suppression of $H_2O_2$-induced oxidative stress by either JNK inhibitor or c-Jun specific antisense transfection was temporary in the cells exposed to glucose oxidase but not to a bolus $H_2O_2$. This was associated with the disruption of death signaling according to the severe and prolonged depletion of reduced glutathione. Overall, these results suggest that $H_2O_2$ may decide differently the mode of cell death by affecting the intracellular redox state of thiol-containing antioxidants, and this depends more closely on the duration exposed to $H_2O_2$ than the concentration of this agent.

Selective Interaction Between Chloroplast β-ATPase and TGB1L88 Retards Severe Symptoms Caused by Alternanthera mosaic virus Infection

  • Seo, Eun-Young;Nam, Jiryun;Kim, Hyun-Seung;Park, Young-Hwan;Hong, Seok Myeong;Lakshman, Dilip;Bae, Hanhong;Hammond, John;Lim, Hyoun-Sub
    • The Plant Pathology Journal
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    • v.30 no.1
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    • pp.58-67
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    • 2014
  • The multifunctional triple gene block protein 1 (TGB1) of the Potexvirus Alternanthera mosaic virus (AltMV) has been reported to have silencing suppressor, cell-to-cell movement, and helicase functions. Yeast two hybrid screening using an Arabidopsis thaliana cDNA library with TGB1 as bait, and co-purification with TGB1 inclusion bodies identified several host proteins which interact with AltMV TGB1. Host protein interactions with TGB1 were confirmed by biomolecular fluorescence complementation, which showed positive TGB1 interaction with mitochondrial ATP synthase delta' chain subunit (ATP synthase delta'), light harvesting chlorophyll-protein complex I subunit A4 (LHCA4), chlorophyll a/b binding protein 1 (LHB1B2), chloroplast-localized IscA-like protein (ATCPISCA), and chloroplast ${\beta}$-ATPase. However, chloroplast ${\beta}$-ATPase interacts only with $TGB1_{L88}$, and not with weak silencing suppressor $TGB1_{L88}$. This selective interaction indicates that chloroplast ${\beta}$-ATPase is not required for AltMV movement and replication; however, TRV silencing of chloroplast ${\beta}$-ATPase in Nicotiana benthamiana induced severe tissue necrosis when plants were infected by AltMV $TGB1_{L88}$ but not AltMV $TGB1_{L88}$, suggesting that ${\beta}$-ATPase selectively responded to $TGB1_{L88}$ to induce defense responses.

Protein-protein Interaction Network Analyses for Elucidating the Roles of LOXL2-delta72 in Esophageal Squamous Cell Carcinoma

  • Wu, Bing-Li;Zou, Hai-Ying;Lv, Guo-Qing;Du, Ze-Peng;Wu, Jian-Yi;Zhang, Pi-Xian;Xu, Li-Yan;Li, En-Min
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.5
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    • pp.2345-2351
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    • 2014
  • Lysyl oxidase-like 2 (LOXL2), a member of the lysyl oxidase (LOX) family, is a copper-dependent enzyme that catalyzes oxidative deamination of lysine residues on protein substrates. LOXL2 was found to be overexpressed in esophageal squamous cell carcinoma (ESCC) in our previous research. We later identified a LOXL2 splicing variant LOXL2-delta72 and we overexpressed LOXL2-delta72 and its wild type counterpart in ESCC cells following microarray analyses. First, the differentially expressed genes (DEGs) of LOXL2 and LOXL2-delta72 compared to empty plasmid were applied to generate protein-protein interaction (PPI) sub-networks. Comparison of these two sub-networks showed hundreds of different proteins. To reveal the potential specific roles of LOXL2- delta72 compared to its wild type, the DEGs of LOXL2-delta72 vs LOXL2 were also applied to construct a PPI sub-network which was annotated by Gene Ontology. The functional annotation map indicated the third PPI sub-network involved hundreds of GO terms, such as "cell cycle arrest", "G1/S transition of mitotic cell cycle", "interphase", "cell-matrix adhesion" and "cell-substrate adhesion", as well as significant "immunity" related terms, such as "innate immune response", "regulation of defense response" and "Toll signaling pathway". These results provide important clues for experimental identification of the specific biological roles and molecular mechanisms of LOXL2-delta72. This study also provided a work flow to test the different roles of a splicing variant with high-throughput data.

Proliferation of Toxoplasma gondii Suppresses Host Cell Autophagy

  • Lee, Youn-Jin;Song, Hyun-Ouk;Lee, Young-Ha;Ryu, Jae-Sook;Ahn, Myoung-Hee
    • Parasites, Hosts and Diseases
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    • v.51 no.3
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    • pp.279-287
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    • 2013
  • Autophagy is a process of cytoplasmic degradation of endogenous proteins and organelles. Although its primary role is protective, it can also contribute to cell death. Recently, autophagy was found to play a role in the activation of host defense against intracellular pathogens. The aims of our study was to investigate whether host cell autophagy influences Toxoplasma gondii proliferation and whether autophagy inhibitors modulate cell survival. HeLa cells were infected with T. gondii with and without rapamycin treatment to induce autophagy. Lactate dehydrogenase assays showed that cell death was extensive at 36-48 hr after infection in cells treated with T. gondii with or without rapamycin. The autophagic markers, LC3 II and Beclin 1, were strongly expressed at 18-24 hr after exposure as shown by Western blotting and RT-PCR. However, the subsequent T. gondii proliferation suppressed autophagy at 36 hr post-infection. Pre-treatment with the autophagy inhibitor, 3-methyladenine (3-MA), down-regulated LC3 II and Beclin 1. The latter was also down-regulated by calpeptin, a calpain inhibitor. Monodansyl cadaverine (MDC) staining detected numerous autophagic vacuoles (AVs) at 18 hr post-infection. Ultrastructural observations showed T. gondii proliferation in parasitophorous vacuoles (PVs) coinciding with a decline in the numbers of AVs by 18 hr. FACS analysis failed to confirm the presence of cell apoptosis after exposure to T. gondii and rapamycin. We concluded that T. gondii proliferation may inhibit host cell autophagy and has an impact on cell survival.

Tazarotene-Induced Gene 1 Enhanced Cervical Cell Autophagy through Transmembrane Protein 192

  • Shyu, Rong-Yaun;Wang, Chun-Hua;Wu, Chang-Chieh;Chen, Mao-Liang;Lee, Ming-Cheng;Wang, Lu-Kai;Jiang, Shun-Yuan;Tsai, Fu-Ming
    • Molecules and Cells
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    • v.39 no.12
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    • pp.877-887
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    • 2016
  • Tazarotene-induced gene 1 (TIG1) is a retinoic acid-inducible protein that is considered a putative tumor suppressor. The expression of TIG1 is decreased in malignant prostate carcinoma or poorly differentiated colorectal adenocarcinoma, but TIG1 is present in benign or well-differentiated tumors. Ectopic TIG1 expression led to suppression of growth in cancer cells. However, the function of TIG1 in cell differentiation is still unknown. Using a yeast two-hybrid system, we found that transmembrane protein 192 (TMEM192) interacted with TIG1. We also found that both TIG1A and TIG1B isoforms interacted and co-localized with TMEM192 in HtTA cervical cancer cells. The expression of TIG1 induced the expression of autophagy-related proteins, including Beclin-1 and LC-3B. The silencing of TMEM192 reduced the TIG1-mediated upregulation of autophagic activity. Furthermore, silencing of either TIG1 or TMEM192 led to alleviation of the upregulation of autophagy induced by all-trans retinoic acid. Our results demonstrate that the expression of TIG1 leads to cell autophagy through TMEM192. Our study also suggests that TIG1 and TMEM192 play an important role in the all-trans retinoic acid-mediated upregulation of autophagic activity.

Identification and Expression Profiles of Six Transcripts Encoding Carboxylesterase Protein in Vitis flexuosa Infected with Pathogens

  • Islam, Md. Zaherul;Yun, Hae Keun
    • The Plant Pathology Journal
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    • v.32 no.4
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    • pp.347-356
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    • 2016
  • Plants protect themselves from pathogen attacks via several mechanisms, including hypersensitive cell death. Recognition of pathogen attack by the plant resistance gene triggers expression of carboxylesterase genes associated with hypersensitive response. We identified six transcripts of carboxylesterase genes, Vitis flexuosa carboxylesterase 5585 (VfCXE5585), Vf-CXE12827, VfCXE13132, VfCXE17159, VfCXE18231, and VfCXE47674, which showed different expression patterns upon transcriptome analysis of V. flexuosa inoculated with Elsinoe ampelina. The lengths of genes ranged from 1,098 to 1,629 bp, and their encoded proteins consisted of 309 to 335 amino acids. The predicted amino acid sequences showed hydrolase like domains in all six transcripts and contained two conserved motifs, GXSXG of serine hydrolase characteristics and HGGGF related to the carboxylesterase family. The deduced amino acid sequence also contained a potential catalytic triad consisted of serine, aspartic acid and histidine. Of the six transcripts, Vf-CXE12827 showed upregulated expression against E. ampelina at all time points. Three genes (VfCXE5585, VfCXE12827, and VfCXE13132) showed upregulation, while others (VfCXE17159, VfCXE18231, and VfCXE47674) were down regulated in grapevines infected with Botrytis cinerea. All transcripts showed upregulated expression against Rhizobium vitis at early and later time points except VfCXE12827, and were downregulated for up to 48 hours post inoculation (hpi) after upregulation at 1 hpi in response to R. vitis infection. All tested genes showed high and differential expression in response to pathogens, indicating that they all may play a role in defense pathways during pathogen infection in grapevines.

Carbon Monoxide Ameliorates 6-Hydroxydopamine-Induced Cell Death in C6 Glioma Cells

  • Moon, Hyewon;Jang, Jung-Hee;Jang, Tae Chang;Park, Gyu Hwan
    • Biomolecules & Therapeutics
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    • v.26 no.2
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    • pp.175-181
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    • 2018
  • Carbon monoxide (CO) is well-known as toxic gas and intrinsic signaling molecule such as neurotransmitter and blood vessel relaxant. Recently, it has been reported that low concentration of CO exerts therapeutic actions under various pathological conditions including liver failure, heart failure, gastric cancer, and cardiac arrest. However, little has been known about the effect of CO in neurodegenerative diseases like Parkinson's disease (PD). To test whether CO could exert a beneficial action during oxidative cell death in PD, we examined the effects of CO on 6-hydroxydopamine (6-OHDA)-induced cell death in C6 glioma cells. Treatment of CO-releasing molecule-2 (CORM-2) significantly attenuated 6-OHDA-induced apoptotic cell death in a dose-dependent manner. CORM-2 treatment decreased Bax/Bcl2 ratio and caspase-3 activity, which had been increased by 6-OHDA. CORM-2 increased phosphorylation of NF-E2-related factor 2 (Nrf2) which is a transcription factor regulating antioxidant proteins. Subsequently, CORM-2 also increased the expression of heme oxygenase-1 and superoxide dismutases (CuZnSOD and MnSOD), which were antioxidant enzymes regulated by Nrf2. These results suggest that CO released by CORM-2 treatment may have protective effects against oxidative cell death in PD through the potentiation of cellular adaptive survival responses via activation of Nrf2 and upregulation of heme oxygenase-1, leading to increasing antioxidant defense capacity.

Antiviral activity of interferon-like cytokine (ILC) produced by head kidney leucocytes of common carp, Cyprinus carpio L (잉어 두신 백혈구에서 생성된 Interferon-like cytokine (ILC)의 항바이러스 활성)

  • Jo, Mi-Yeong;Kim, Eun-Jeon;Im, Sang-Gu;Kim, Jun-U;Park, Su-Il
    • Journal of fish pathology
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    • v.17 no.2
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    • pp.75-82
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    • 2004
  • Interferons are kinds of cytokines that play an important role in antiviral defense mechanisms during viral infection by converting cells to synthesize proteins that inhibit viral replication. In the present study, an antiviral response against Spring viremia of carp virus (SVCV) was developed in common carp, Cyprinus carpio following stimulation with the potent interferon inducer, poly inosinic : cytidylic acid (poly I:C). Poly I:C injected fish showed lower cumulative mortalities against SVCV than untreated fish did. Moreover, in vitro study showed that head kidney leucocytes (HKLs) produced an interferon-like cytokine (ILC) after stimulation with poly I:C. According cytopathic effect reduction (CPER) assay to examine antiviral activity of crude ILC, the capacity of HKLs for ILC production was highest at 1×$10^6$cells/ml and significantly enhanced when treated with 20~50$\mu{g}$/ml of poly I:C. The optimal temperature and concentration of FBS to induce the highest ILC production were $20^\circ{C}$ and 5%, respectively.