• Journal of Life Science
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• v.30 no.4
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• pp.402-409
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• 2020

Nervous necrosis virus (NNV) contains a bi-segmented viral genome, RNA1 (3.4 kb, RdRp), and RNA2 (1.4 kb, capsid protein) in a small particle (25 nm). Despite its extremely compact size, NNV has caused serious damage by infecting approximately 120 fish species worldwide since it was first reported in the late 1980s. In order to minimize the damage caused by NNV infection and develop effective vaccines, it is necessary to understand the intra cellular signaling system according to NNV infection. NNV infection induces cell cycle arrest at the G1 phase via the p53-dependent pathway to use the cellular system for its replication. Otherwise, host cells recognize NNV infection through the RIG-1-like receptor (RLR) signaling pathway to control the virus and infected cells, and then ISGs required for antiviral action are activated via the IFN signaling pathway. Moreover, apoptosis of infected cells is triggered by the unfolded protein response (UPR) through ER stress and mitochondria-mediated cell death. Cell signaling studies on the NNV infection mechanisms are still at an early stage and many pathways have yet to be identified. Understanding the various disease-specific cellular signaling systems associated with NNV infection is essential for rapid and accurate diagnosis and vaccine development.

• Journal of Plant Biotechnology
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• v.37 no.3
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• pp.327-336
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• 2010

Cysteine proteases have been known as a critical factor in plant defense mechanisms in pineapple, papaya, or wild fig. Papain or ficin is one kind of cysteine proteases that shows toxic effects to herbivorous insects and pathogenic bacteria. However, resistance to bacterial soft rot of plants genetically engineered with cysteine protease has been little examined thus far. We cloned a cysteine protease cDNA from Ananas comosus and introduced the gene into Chinese cabbage (Brassica rapa) under the control of the cauliflower mosaic virus 35S promoter. The transgene was stably integrated and actively transcribed in transgenic plants. In comparisons with wild-type plants, the $T_2$ and $T_3$ transgenic plants exhibited a significant increase in endo-protease activity in leaves and enhanced resistance to bacterial soft rot. A cDNA microarray analysis revealed that several genes were more abundantly transcribed in the transgenic than in the wild type. These genes encode a glyoxal oxidase, PR-1 protein, PDF1, protein kinase, LTP protein, UBA protein and protease inhibitor. These results suggest an important role for cysteine protease as a signaling regulator in biotic stress signaling pathways, leading to the build-up of defense mechanism to pathogenic bacteria in plants.

• The Plant Pathology Journal
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• v.27 no.3
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• pp.272-279
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• 2011

Root colonization of Arabidopsis thaliana with Pseudomonas chlororaphis O6 induces systemic tolerance against diverse pathogens, as well as drought and salt stresses. In this study, we demonstrated that 11 genes in the leaves were up-regulated, and 5 genes were down-regulated as the result of three- to five-days root colonization by P. chlororaphis O6. The identified priming genes were involved in cell signaling, transcription, protein synthesis, and degradation. In addition, expression of selected priming genes were induced in P. chlororaphis O6-colonized plants subjected to water withholding. Genes encoding defense proteins in signaling pathways regulated by jasmonic acid and ethylene, such as VSP1 and PDF1.2, were additional genes with enhanced expression in the P. chlororaphis O6-colonized plants. This study indicated that the expression of priming genes, as well as genes involved in jasmonic acid- and ethylene-regulated genes may play an important role in the systemic induction of both abiotic and biotic stress due to root colonization by P. chlororaphis O6.

• BMB Reports
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• v.47 no.2
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• pp.51-59
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• 2014

Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy.

• Molecules and Cells
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• v.39 no.1
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• pp.31-39
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• 2016

The peroxiredoxins (Prxs) constitute a very large and highly conserved family of thiol-based peroxidases that has been discovered only very recently. We consider here these enzymes through the angle of their discovery, and of some features of their molecular and physiological functions, focusing on complex phenotypes of the gene mutations of the 2-Cys Prxs subtype in yeast. As scavengers of the low levels of $H_2O_2$ and as $H_2O_2$ receptors and transducers, 2-Cys Prxs have been highly instrumental to understand the biological impact of $H_2O_2$, and in particular its signaling function. 2-Cys Prxs can also become potent chaperone holdases, and unveiling the in vivo relevance of this function, which is still not established, should further increase our knowledge of the biological impact and toxicity of $H_2O_2$. The diverse molecular functions of 2-Cys Prx explain the often-hard task of relating them to peroxiredoxin genes phenotypes, which underscores the pleiotropic physiological role of these enzymes and complex biologic impact of $H_2O_2$.

• Microbiology and Biotechnology Letters
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• v.47 no.1
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• pp.1-10
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• 2019

Saline soils comprise more than half a billion hectares worldwide. Thus, they warrant attention for their efficient, economical, and environmentally acceptable management. Halophytes are being progressively utilized for human benefits. The halophyte microbiome contributes significantly to plant performance and can provide information regarding complex ecological processes involved in the osmoregulation of halophytes. Microbial communities associated with the rhizosphere, phyllosphere, and endosphere of halophytes play an important role in plant health and productivity. Members of the plant microbiome belonging to domains Archaea, Bacteria, and kingdom Fungi are involved in the osmoregulation of halophytes. Halophilic microorganisms principally use compatible solutes, such as glycine, betaine, proline, trehalose, ectoine, and glutamic acid, to survive under salinity stress conditions. Plant growth-promoting rhizobacteria (PGPR) enhance plant growth and help to elucidate tolerance to salinity. Detailed studies of the metabolic pathways of plants have shown that plant growth-promoting rhizobacteria contribute to plant tolerance by affecting the signaling network of plants. Phytohormones (indole-3-acetic acid and cytokinin), 1-aminocyclopropane-1-carboxylic acid deaminase biosynthesis, exopolysaccharides, halocins, and volatile organic compounds function as signaling molecules for plants to elicit salinity stress. This review focuses on the functions of plant microbiome and on understanding how the microorganisms affect halophyte health and growth.

• Herbal Formula Science
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• v.30 no.3
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• pp.137-143
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• 2022

Objectives : Brain-Liver axis is an important target of the chronic human diseases. Hepatic steatosis is one of the most famous disorders in the chronic diseases. This study investigated the moderating effect of beneficial herbs on the fat accumulation, which is mediated by the LXR alpha-SREBP-1c signaling pathway. Methods : In order to confirm the SREBP-1c inhibitory effect, we performed immonoblotting ananlysis using HepG2 cells and Huh 7 cells treated by T0901317, the ligand of LXRα. Results : Forsythiae suspensa water extract (FSE) was not cytotoxicity in cell lines. FSE inhibited SREBP-1c protein expression in HepG2 and Huh7 cells induced by T0901317. In addition, FSE increased the phosphorylation of LKB1, which is associated with LXR-related pathway in HepG2 and Huh 7 cells. Conclusions : These results showed that FSE activated LKB1 to suppress SREBP-1c, which protects the cells against oxidative stress.

• Molecules and Cells
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• v.37 no.6
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• pp.435-440
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• 2014

Hemodynamic shear stress, the frictional force acting on vascular endothelial cells, is crucial for endothelial homeostasis under normal physiological conditions. When discussing blood flow effects on various forms of endothelial (dys)function, one considers two flow patterns: steady laminar flow and disturbed flow because endothelial cells respond differently to these flow types both in vivo and in vitro. Laminar flow which exerts steady laminar shear stress is atheroprotective while disturbed flow creates an atheroprone environment. Emerging evidence has provided new insights into the cellular mechanisms of flowdependent regulation of vascular function that leads to cardiovascular events such as atherosclerosis, atherothrombosis, and myocardial infarction. In order to study effects of shear stress and different types of flow, various models have been used. In this review, we will summarize our current views on how disturbed flow-mediated signaling pathways are involved in the development of atherosclerosis.

• Journal of Breast Cancer
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• v.21 no.4
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• pp.354-362
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• 2018

Cellular stress severely disrupts endoplasmic reticulum (ER) function, leading to the abnormal accumulation of unfolded or misfolded proteins in the ER and subsequent development of endoplasmic reticulum stress (ERS). To accommodate the occurrence of ERS, cells have evolved a highly conserved, selfprotecting signal transduction pathway called the unfolded protein response. Notably, ERS signaling is involved in the development of a variety of diseases and is closely related to tumor development, particularly in breast cancer. This review discusses recent research regarding associations between ERS and tumor metastasis. The information presented here will help researchers elucidate the precise mechanisms underlying ERS-mediated tumor metastasis and provide new directions for tumor therapies.

• International Journal of Vascular Biomedical Engineering
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• v.2 no.2
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• pp.1-9
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• 2004

The history of studies in biology regarding reactive oxygen species (ROS) is approximately 40 years. During the initial 30 years, it appeared that these studies were mainly focused on the toxicity of ROS. However, recent studies have identified another action regarding oxidative signaling, other than toxicity of ROS. Basically, it is suggested that ROS are reactive, and degenerate to biomolecules such as DNA and proteins, leading to deterioration of cellular functions as an oxidative stress. On the other hand, recent studies have shown that ROS act as oxidative signaling in cells, resulting in various gene expressions. Recently ROS emerged as critical signaling molecules in cardiovascular research. Several studies over the past decade have shown that physiological effects of vasoactive factors are mediated by these reactive species and, conversely, that altered redox mechanisms are implicated in the occurrence of metabolic and cardiovascular diseases ROS is a collective term often used by scientist to include not only the oxygen radicals($O2^{-{\cdot}},\;{^{\cdot}}OH$), but also some non-radical derivatives of oxygen. These include hydrogen peroxide, hypochlorous acid (HOCl) and ozone (O3). The superoxide anion ($O2^{-{\cdot}}$) is formed by the univalent reduction of triplet-state molecular oxygen ($^3O_2$). Superoxide dismutase (SOD)s convert superoxide enzymically into hydrogen peroxide. In biological tissues superoxide can also be converted nonenzymically into the nonradical species hydrogen peroxide and singlet oxygen ($^1O_2$). In the presence of reduced transition metals (e.g., ferrous or cuprous ions), hydrogen peroxide can be converted into the highly reactive hydroxyl radical (${^{\cdot}}OH$). Alternatively, hydrogen peroxide may be converted into water by the enzymes catalase or glutathione peroxidase. In the glutathione peroxidase reaction glutathione is oxidized to glutathione disulfide, which can be converted back to glutathione by glutathione reductase in an NADPH-consuming process.