• Journal of Plant Biology
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• v.38 no.3
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• pp.243-250
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• 1995

Involvement of calcium in signal transduction of salt stress was investigated in 1.7 M NaCl adapted Dunaliella salina, extremely halotolerant, unicellular green alga. When hyperosmotic (3.4 M NaCl) or Hypoosmotic (0.8 M NaCl) stress was treated, extracellular calcium was influxed in or intracellular calcium effluxed from D. salina, respectively, and these fluxes were proportional to the degree of stress. This might indicate indirectly that the change of calcium level occurred within the cells. In addition, the change of calcium flux was ahead of glycerol synthesis which has been known as the physiological response to salt stress. Osmoregulation was affected byextracellular calcium concentration, and increase of glycerol content as an osmoticum was inhibited about 50% by treatment of TFP and W-7 known as calmodulin specific inhibitors. Furthermore, in the case of the hyperosmotic stressed cells, the amount of 21 kD and 39 kD protein appeared to be calcium binding protein were increased. Among these, the 39 kD protein was detected only in the hyperosmotic stressed cells. The results obtained in the present work suggest that the possibility of calcium as a second messenger in the transduction of salt stress signal exists in the osmoregulation system of D. salina.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3359-3362
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• 2014

Increasing attention is being devoted to the mechanisms by which cells receive signals and then translate these into decisions for growth, death, or migration. Recent findings have presented significant breakthroughs in developing a deeper understanding of the activation or repression of target genes and proteins in response to various stimuli and of how they are assembled during signal transduction in cancer cells. Detailed mechanistic insights have unveiled new maps of linear and integrated signal transduction cascades, but the multifaceted nature of the pathways remains unclear. Although new layers of information are being added regarding mechanisms underlying ovarian cancer and how polymorphisms in VDR gene influence its development, the findings of this research must be sequentially collected and re-interpreted. We divide this multi-component review into different segments: how vitamin D modulates molecular network in ovarian cancer cells, how ovarian cancer is controlled by tumor suppressors and oncogenic miRNAs and finally how vitamin D signaling regulates miRNA expression. Intra/inter-population variability is insufficiently studied and a better understanding of genetics of population will be helpful in getting a step closer to personalized medicine.

• Journal of Photoscience
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• v.5 no.2
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• pp.73-81
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• 1998

Light signals constitute major factors in regulating gene expression and morphogenesis in plants and fungi. Phytochrome A and B were well characterized red and far-red light receptors in plants. Red light signals increased the phosphorylation of 18 kDa protein, which was identified to be nucleoside diphosphate (NDP) kinase. The NDP kinase catalyzed autophosphorylation and had a protein kinase activity similar to MAP (mitogen activated protein) kinase. As candidates for blue light photoreceptors, cDNAs for CRY1 and CRY2 were isolated. The N-teminal regions of these proteins showed a high hornology to DNA photolyase. The 120 kDa protein first detected in Pisurn sativurn, which showed blue light induced phosphorylation was also detected in Arabidopsis thaliana. The 120 kDa protein was encoded by the nphl gene, which regulated positive phototropism of the plant. In Neurospora crassa, blue light irradiation of the membrane fraction prepared from roycelia stimulated the phosphorylation of the 15 kDa protein, which was also identifmd to be an NDP kinase. Recent progress in understanding early events in light signal transduction mainly in Pisum sativum Alaska, Arabidopsis thaliana and Neurospora crassa was summarized.

• Journal of Photoscience
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• v.4 no.1
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• pp.23-30
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• 1997

Leaf movements in nyctinastic plants are produced by changes in the turgor of extensor and flexor cells, collectively called motor cells, in opposing regions of the leaf movement organ, the pulvinus. In Samanea saman, a tropical tree of the legume family, extensor cells shrink and flexor cells swell to bend the pulvinus and fold the leaf at night, whereas extensor cells swell and flexor cells shrink to straighten the pulvinus and extend the leaf in the daytime. These changes are caused by ion fluxes primarily of potassium and chloride, across the plasma membrane of the motor cells. These ion fluxes are regulated by exogenous light signals and an endogenous biolgical clock. Inward-directed K$^+$ channels are closed in extensor and open in flexor cells in the dark period, while these channels are open in extensor and closed in flexor cells in the light period. Blue light opens the closed K$^+$ channels in extensor and closes the open them in flexor cells during darkness. Illumination of red light followed by darkness induces to open the closed K$^+$ channels in flexor and to close the open K$^+$ channels in extensor cells in the light. The dynamics of K$^+$ channels in motor cells that are controlled by light signals are consistent with the behavior of the pulvini in intact plants. Therefore, these cell types are an attractive model system to elucidate regulations of ion transports and their signal transduction pathways in plants. This review is focused on light-controlled ion movements and regulatory mechanisms involved in phosphoinositide signaling in leaf movements in nyctinastic plants.

• Natural Product Sciences
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• v.12 no.4
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• pp.175-192
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• 2006

Screening for the cytotoxicity from plant origin is the first stage for anti-cancer drug development. A variety of terpenoids with exomethylene, epoxide, allyl, $\alpha,\beta-unsaturated$ carbonyl, acetylenes, and $\alpha-methylene-\gamma-lactone$ induces apoptosis and/or differentiation as well as cytotoxicity through the ROS signal transduction pathways. These are found among monoterpenes, sesquiterpenes, triterpenes, flavonoids, coumarins, diarylheptanoids, and even organosulfuric compounds. The most essential characteristics of natural cytotoxic substances is to possess the strong electrophilicity that is susceptible to nucleophilic biomolecules in the cell. Thiol-reductants and superoxide dismutase can block or delay apoptosis. Thus, ROS and the resulting cellular redox-potential changes can be parts of the signal transduction pathway during apoptosis. Disturbance of the balance of oxireduction by the pigment of natural quinones also caused the induction of the differentiation and apoptosis. Saponins with the cytotoxicity are restricted to their monodesmosides, rather than to bisdesmosides. Those saponins exhibited calcium ion-mediated apoptosis in addition to cytotoxicity whereas they showed also differentiation without extracellular calcium ion. The properties on cytotoxicity, apoptosis, and differentiation were assumed to depend on resultant oxidative stress to the cells. In this review, we describe a spectrum of cytotoxic compounds with various action mechanisms.

• 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.

• The Korean Journal of Food And Nutrition
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• v.24 no.2
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• pp.258-267
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• 2011

14-3-3 is a highly conserved, ubiquitously expressed protein family. It associates with diverse cellular proteins through its specific phosphoserine/phosphothreonine-binding activity and thus contributes to the regulation of crucial cellular processes such as metabolism, signal transduction, cell-cycle control, apoptosis, protein trafficking, transcription and stress responses. This study aims to determine changes in levels of 14-3-3 isoforms and 14-3-3 - associated proteins in Helicobacter pylori(H. pylori)-infected gastric epithelial AGS cells. AGS cells were stimulated with H. pylori(NCTC 11637) at the ratio of 300:1(bacterium:cell). Western blot analysis revealed that 14-3-3 $\sigma$ was elevated at 3 hr after H. pylori treatment. Other isoforms were not significantly affected by H. pylori infection. Using immunoprecipitation to 14-3-3 $\sigma$, followed by proteomic analysis, we found that S phase kinase associated protein isoform 2 bound to 14-3-3 $\sigma$ has increased. In contrast, three proteins (DEAD-box polypeptide 3, heterogeneous nuclear ribonucleoprotein H2 and WD repeat-containing protein isoform 1) bound to 14-3-3 decreased by H. pylori infection. Our results suggest that 14-3-3 may play an important regulatory role in H. pylori-induced signal transduction in gastric epithelial cells.

• Molecules and Cells
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• v.39 no.3
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• pp.186-194
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• 2016

Epidemiological evidence suggests that bone is especially sensitive to oxidative stress, causing bone loss in the elderly. Previous studies indicated that human amnion-derived mesenchymal stem cells (HAMSCs), obtained from human amniotic membranes, exerted osteoprotective effects in vivo. However, the potential of HAMSCs as seed cells against oxidative stress-mediated dysfunction is unknown. In this study, we systemically investigated their antioxidative and osteogenic effects in vitro. Here, we demonstrated that HAMSCs significantly promoted the proliferation and osteoblastic differentiation of $H_2O_2$-induced human bone marrow mesenchymal stem cells (HBMSCs), and down-regulated the reactive oxygen species (ROS) level. Further, our results suggest that activation of the ERK1/2 MAPK signal transduction pathway is essential for both HAMSCs-mediated osteogenic and protective effects against oxidative stress-induced dysfunction in HBMSCs. U0126, a highly selective inhibitor of extracellular ERK1/2 MAPK signaling, significantly suppressed the antioxidative and osteogenic effects in HAMSCs. In conclusion, by modulating HBMSCs, HAMSCs show a strong potential in treating oxidative stress- mediated bone deficiency.

• BMB Reports
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• v.38 no.3
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• pp.281-289
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• 2005

Tumor necrosis factor (TNF) signaling is mediated via two distinct receptors, TNFR2 and TNFR1, which shows partially overlapping signaling mechanisms and biological roles. In the present study, TNFR2 and TNFR1 signal transduction mechanisms involved in activation of $NF{\kappa}B$ and CMV promoter-enhancer were compared with respect to their susceptibility towards inhibitors of intracellular signaling. For this, we used SW480 cells, where we have shown that TNF-signaling can occur independently through each of the two receptors. The TNFR1 response was inhibited by D609, bromophenacyl bromide (BPB), nordihydroguararetic acid (NDGA), and by sodium salicylate, while TNFR2-mediated activation of $NF{\kappa}B$ and CMV promoter-enhancer was resistant to these compounds. The signaling mechanisms known to be affected by these inhibitors include phospholipases as well as redox- and pH-sensitive intracellular components. Our results imply that TNFR2 signaling involved in $NF{\kappa}B$ activation proceeds independently of these inhibitor-sensitive signaling components, indicating distinct signaling pathways not shared with TNFR1.

• YAKHAK HOEJI
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• v.39 no.6
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• pp.661-665
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• 1995

Ginsenoside-Rg$_{1}$(G-Rg$_{1}$) has been shown to stimulate DNA synthetic activity in SK-HEP-1 cells. This study was therefore designed to determine in SK-HEP-1 cells whether the stimulatory effect of G-Rg$_{1}$ may be mediated by protein kinase C (PKC) which is known to play a key role in the signal transduction pathway leading to the cell proliferation. Using the tn situ PKC assay method, the PKC enzyme activity was determined in SK-HEP-1 cell cultures in response to G-Rg$_{1}$ at 3*10$^{-5}$ M or phorbol 12-myristate 13-acetate(PMA) at 10$^{-6}$ M which in the enzyme activity by 1.5- and 7-fold, respectively. Furthermore, G-Rg$_{1}$, was also able to synergistically increase the enzyme activity by 11-fold m the cell cultures in the presence of PMA. These stimulatory effects of G-Rg$_{1}$ or PMA on the DNA synthetic activity and the PKC activity were ablished by a specific PKC inhibitor, GF109203X. These results suggest that the stimulatory effect of G-Rg$_{1}$ on the DNA synthetic activity may be partly due to stimulation of PKC-mediated signal transduction pathway leading to the proliferation of SK-HEP-1 cells.