• Korean Journal of Veterinary Research
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• v.34 no.1
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• pp.25-36
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• 1994

The inward tail current after a short depolarizing pulse has been known as Na-Ca exchange current activated by intracellular calcium which forms late plateau of the action potential in rabbit atrial myocytes. Chloride conductance which is also dependent upon calcium concentration has been reported as a possible tail current in many other excitable tissues. Thus, in order to investigate the exsitance of the calcium activated chloride current and its contribution to tail current, whole cell voltage clamp measurement has been made in single atrial cells of the rabbit. The current was recorded during repolarization following a brief 2 ms depolarizing pulse to +40mV from a holding potential of -70mV. When voltage-sensitive transient outward current was blocked by 2 mM 4-aminopyridine or replacement potassium with cesium, the tail current were abolished by ryanodine$(1{\mu}M)$ or diltiazem$(10{\mu}M)$ and turned out to be calcium dependent. The magnitudes of the tail currents were increased when intracellular chloride concentration was increased to 131 mM from 21 mM. The current was decreased by extracellular sodium reduction when intracellular chloride concentration was low(21 mM), but it was little affected by extracellular sodium reduction when intracellual chloride concentration was high(131 mM). The current-voltage relationship of the difference current before and after extracellular sodium reduction, shows an exponential voltage dependence with the largest magnitude of the current occurring at negative potentials, with is similar to current-voltage relationship at negative potentials, which is similar to current-voltage relationship of Na-Ca exchange current. The current was also decreased by $10{\mu}M$ niflumic acid and 1 mM bumetanide, which is well known anion channel blockers. The reversal potentials shifted according to changes in chloride concentration. The current-voltage relationships of the niflumic acid-sensitive currents in high and low concentration of chloride were well fitted to those predicted as chloride current. From the above results, it is concluded that calcium activated chloride component exists in the tail current with Na-Ca exchange current and it shows the reversal of tail current. Therefore it is thought that in the physiologic condition it leads to rapid end of action potential which inhibits calcium influx and it contributes to maintain the low intracellular calcium concentration with Na-Ca exchange mechanism.

• Korean Journal of Medicinal Crop Science
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• v.20 no.2
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• pp.124-128
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• 2012

When ginseng seedlings are cultured in paddy fields, quality degradation and yield reduction are induced by severe plant loss with chlorosis on leaves occurred physiological disorder by excessive salt and poor drainage, rusty-root occurrence, and root rot etc. Accordingly, in order to solve these problems, this study was performed to investigate the treatment method, concentrations and time of activated ion calcium as environment-friendly agricultural materials. Activated ion calcium is an enriched and purified water-soluble mineral calcium component for absorbing quickly into plant as a highly functional calcium and it is an alkaline calcium of 37% (370 $m{\ell}$/1 ${\ell}$) concentration with pH 13. Treatment method was that ginseng seeds were sown after removing water in the shade after seed immersion for 1 minute with active ion calcium of 20-fold diluted solution, and then irrigated $4{\ell}$ per 3.3 $m^2$ with 200-fold, 400-fold, and 600-fold diluted solution before emergence on late March, and supplied 1 time on leaves with 500-fold diluted solution in June and July respectively. The disease rate by treatment of activated ion calcium was that on the treatment of soil irrigated with 200-fold diluted solution compared to non-treated soil, damping-off was 33%, anthracnose was 100% reduced and the occurrence rate of rusty-root was 30% reduced. In addition, when active ion calcium of 200-fold diluted solution were soil irrigated, first and second grade ginseng were respectively 26% and 22% produced more, compared with control.

• BMB Reports
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• v.31 no.5
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• pp.468-474
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• 1998

Membrane depolarization in PC12 cells induces calcium influx via an L-type voltage-sensitive calcium channel (L-VSCC) and increases intracellular free calcium, which leads to tyrosine phosphorylation of epidermal growth factor (EGF) receptor and the associated adaptor protein, She. This activated EGF receptor complex then can activate mitogen-activated protein (MAP) kinase, as in nerve growth factor (NGF) receptor activation. In the present study, we investigated the role of EGF receptor in the signaling pathway initiated by membrane depolarization of PC12 cells. Prolonged membrane depolarization induced phosphorylation of extracellular signal-regulated kinase (ERK) within 1 min in undifferentiated PC12 cells. Pretreatment of PC12 cells with the calcium chelator EGTA abolished depolarization-stimulated ERK phosphorylation, but NGF-induced phosphorylation of ERK was not affected. The chronic treatment of phorbol ester, which down-regulated the activity of protein kinase C (PKC), did not affect the phosphorylation of ERK upon depolarization. In the presence of an inhibitor of EGF receptor, neither depolarization nor calcium ionophore increased the level of ERK phosphorylation. These data imply that the EGF receptor is functionally necessary to activate ERK and neurite outgrowth in response to the prolonged depolarization in PC12 cells, and also that PKC is apparently not involved in this signaling pathway.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.83-92
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• 1988

Although the release of lysosomal enzymes from activated PMN leukocyte can be regulated by intracellular cyclic nucleotide levels, other responses of PMN leukocyte according to the binding of neurotransmitters to either ${\beta}$-adrenergic or muscarinic receptors are still not clarified. In addition, the function of PMN leukocyte mediated by ${\alpha}$-adrenergic receptors is uncertain. Atropine, phentolamine and propranolol inhibited calcium uptake, superoxide generation, NADPH oxidase activity and phagocytic activity in activated PMN leukocyte, whereas carbachol and isoproterenol slightly further stimulated the responses of activated cells. Either carbachol or isoproterenol stimulated superoxide generation was inhibited by their antagonists, atropine and propranolol, respectively. The response of activated PMN leukocyte was inhibited by chlorpromazine, verapamil and dantrolene but slightly stimulated by lithium. On the other hand, chlorpromazine and dibucaine did not affect NADPH oxidase activity. Atropine, phentolamine and propranolol suppressed the calcium dependent phagocytic activity. Thus, the results suggest that atropine, phentolamine and propranolol may inhibit superoxide generation in activated PMN leukocyte by the inhibition of calcium influx and by their direct action on the NADPH oxidase system which is associated with autonomic receptors.

• Biomolecules & Therapeutics
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• v.31 no.1
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• pp.59-67
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• 2023

Thrombin is a serine protease that participates in a variety of biological signaling through protease-activated receptors. Intestinal myofibroblasts play central roles in maintaining intestinal homeostasis. In this study, we found that thrombin-induced apoptosis is mediated by the calcium-mediated activation of cytosolic phospholipase A₂ in the CCD-18Co cell. Thrombin reduced cell viability by inducing apoptosis and proteinase-activated receptor-1 antagonist attenuated thrombin-induced cell death. Endogenous ceramide did not affect the cell viability itself, but a ceramide-mediated pathway was involved in thrombin-induced cell death. Thrombin increased intracellular calcium levels and cytosolic phospholipase A₂ activity. The ceramide synthase inhibitor Fumonisin B1, intracellular calcium chelator BAPTA-AM, and cytosolic phospholipase A₂ inhibitor AACOCF₃ inhibited thrombin-induced cell death. Thrombin stimulated arachidonic acid release and reactive oxygen species generation, which was blocked by AACOCF₃, BAPTA-AM, and the antioxidant reagent Trolox. Taken together, thrombin triggered apoptosis through calcium-mediated activation of cytosolic phospholipase A₂ in intestinal myofibroblasts.

• ALGAE
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• v.36 no.4
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• pp.315-326
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• 2021

Ion channels are membrane protein complexes mediating passive ion flux across the cell membranes. Every organism has a certain set of ion channels that define its physiology. Dinoflagellates are ecologically important microorganisms characterized by effective physiological adaptability, which backs up their massive proliferations that often result in harmful blooms (red tides). In this study, we used a bioinformatics approach to identify homologs of known ion channels that belong to 36 ion channel families. We demonstrated that the versatility of the dinoflagellate physiology is underpinned by a high diversity of ion channels including homologs of animal and plant proteins, as well as channels unique to protists. The analysis of 27 transcriptomes allowed reconstructing a consensus ion channel repertoire (channelome) of dinoflagellates including the members of 31 ion channel families: inwardly-rectifying potassium channels, two-pore domain potassium channels, voltage-gated potassium channels (K_v), tandem K_v, cyclic nucleotide-binding domain-containing channels (CNBD), tandem CNBD, eukaryotic ionotropic glutamate receptors, large-conductance calcium-activated potassium channels, intermediate/small-conductance calcium-activated potassium channels, eukaryotic single-domain voltage-gated cation channels, transient receptor potential channels, two-pore domain calcium channels, four-domain voltage-gated cation channels, cation and anion Cys-loop receptors, small-conductivity mechanosensitive channels, large-conductivity mechanosensitive channels, voltage-gated proton channels, inositole-1,4,5-trisphosphate receptors, slow anion channels, aluminum-activated malate transporters and quick anion channels, mitochondrial calcium uniporters, voltage-dependent anion channels, vesicular chloride channels, ionotropic purinergic receptors, animal volage-insensitive cation channels, channelrhodopsins, bestrophins, voltage-gated chloride channels H⁺/Cl^- exchangers, plant calcium-permeable mechanosensitive channels, and trimeric intracellular cation channels. Overall, dinoflagellates represent cells able to respond to physical and chemical stimuli utilizing a wide range of G-protein coupled receptors- and Ca²⁺-dependent signaling pathways. The applied approach not only shed light on the ion channel set in dinoflagellates, but also provided the information on possible molecular mechanisms underlying vital cellular processes dependent on the ion transport.

• International Journal of Oral Biology
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• v.40 no.4
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• pp.211-216
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• 2015

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium ($BK_{ca}$) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of $Ca^{2+}$ that induces $Ca^{2+}$-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective $BK_{Ca}$ channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove $Ca^{2+}$ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through $BK_{ca}$ channels, which are activated by intracellular $Ca^{2+}$ increase via activation of RyR of $Ca^{2+}$ stores.

• Journal of the Korean Institute of Electrical and Electronic Material Engineers
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• v.19 no.11
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• pp.1020-1024
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• 2006

Europium$(Eu^{2+}\;or\;Eu^{3+})$-activated calcium aluminium silicate phosphors were synthesized for the first time and the structures and luminescence characteristics of these phosphors were investigated. The phosphors in this study emitted blue, green, and even red light depending on the starting milterials and annealing conditions for synthesis. In addition, the structure was also changed when the different starting materials were used. When $CaCO_3$ was used as a starting material, tetragonal $Ca_2Al_2SiO_7$ was formed. However, pure green light was emitted when the annealing was conducted in reduced atmosphere and red one was emitted by annealing in air. In the case of $CaSiO_3$ as a starting material, triclinic $CaAl_2Si_2O_8$ was formed and only pure blue emission was observed. Moreover, this blue phosphor exhibited higher intensity than that of commercial YAG:Ce phosphor, which showed the possibility of application on the phosphor for new light source such as a UV-LED.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2006.06a
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• pp.32-35
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• 2006

For the white UV-LED applications, $Eu^{2+}$-activated calcium aluminium silicate phosphors were synthesized for the first time and the structures and luminescence characteristics of these phosphors were investigated. The phosphors in this study emitted blue. green or blue-green light depending on the starting materials for synthesis. In addition, the structure was also changed when the different starting materials were used. When CaO and $CaCO_3$ was used as a starting material. tetragonal $Ca_2Al_2SiO_7$ was formed and blue-green and pure green light was emitted. respectively. However. in the case of $CaSiO_3$, triclinic $CaAl_2Si2O_8$ was formed and only pure blue emission was detected. The maximum emission intensity was obtained from $CaAl_2Si_2O_8:Eu^{2+}$ phosphors, which intensity was about 1.4 times higher than that of YAG:$Ce^{3+}$ phosphor used for blue LED.

• The Korean Journal of Pharmacology
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• v.2 no.1 s.2
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• pp.31-40
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• 1966

The microsomal fraction is isolated from rabbit heart and skeletal muscle. The fraction is found to contain the $Na^+$-and $K^+$-activated ATPase. The maximal ATPase activity is obtained in $Na^+$ and $K^+$ concentration of 100 mM. Calcium itself stimulates the $Na^+$-and $K^+$-activated portion of ATPase in the presence of $Mg^{++}$. However, calcium does not stimulate ATPase in the absence of $Mg^{++}$.