• Korean Journal of Fisheries and Aquatic Sciences
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• v.52 no.2
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• pp.159-172
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• 2019

This study investigated the effects of dietary monobasic potassium phosphate (MKP) on the growth of the far eastern catfish Silurus asotus and four leafy vegetables in a hybrid biofloc technology aquaponic system. To an experimental diet containing 45% protein and 7% lipid, 1, 2, 3 or 4% MKP was added and was designated as MKP1, MKP2, MKP3, and MKP4, respectively. The optimum MKP levels were determined for the growth of fish and four leafy vegetables over 10 weeks. After the 10-week feeding trial, weight gain, feed efficiency, specific growth rate and protein efficiency ratio were higher in the fish groups fed MKP2 and MKP3 than in the other groups (P<0.05). The growth of the four leafy vegetables was also higher in the fish groups fed MKP2 and MKP3. Water quality [dissolved oxygen, pH, water temperature, electrical conductivity, turbidity, total ammonia nitrogen (TAN), $NO_2-N$, $NO_3-N$ and $PO_4-P$] was measured six times a week using a portable water quality meter and reagent measurements. The TAN (4.58-20.40 mg/L), $NO_3-N$ (24.12-52.40 mg/L) and $PO_4-P$ (20.38-48.48 mg/L) levels increased with time, while the $NO_2-N$ level remained below 0.1 mg/L throughout the study.

• Natural Product Sciences
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• v.15 no.1
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• pp.32-36
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• 2009

Glutamate causes neurotoxicity through formation of reactive oxygen species and activation of mitogen-activated protein kinase (MAPK) pathways. MAPK phosphatase-1 (MKP-1) is one of the phosphatases responsible for dephosphorylation/deactivation of three MAPK families: the extracellular signal-regulated kinase-1/2 (ERK-1/2), the c-Jun N-terminal kinase-1/2 (JNK-1/2), and the p38 MAPK. In this report, the potential involvement of MKP-1 in neuroprotective effects of curcumin, the active ingredient of turmeric (Curcuma longa), was examined using HT22 cells. Glutamate caused cell death and activation of ERK-1/2 but not p38 MAPK or JNK-1/2. Blockage of ERK-1/2 by its inhibitor protected HT22 cells against glutamate-induced toxicity. Curcumin attenuated glutamate-induced cell death and ERK-1/2 activation. Interestingly, curcumin induced MKP-1 activation. In HT22 cells transiently transfected with small interfering RNA against MKP-1, curcumin failed to inhibit glutamate-induced ERK-1/2 activation and to protect HT22 cells from glutamate-induced toxicity. These results suggest that curcumin can attenuate glutamate-induced neurotoxicity by activating MKP-1 which acts as the negative regulator of ERK-1/2. This novel pathway may contribute to and explain at least one of the neuroprotective actions of curcumin.

• Molecules and Cells
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• v.44 no.10
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• pp.710-722
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• 2021

Hypoxia, or low oxygen tension, is a hallmark of the tumor microenvironment. The hypoxia-inducible factor-1α (HIF-1α) subunit plays a critical role in the adaptive cellular response of hypoxic tumor cells to low oxygen tension by activating gene-expression programs that control cancer cell metabolism, angiogenesis, and therapy resistance. Phosphorylation is involved in the stabilization and regulation of HIF-1α transcriptional activity. HIF-1α is activated by several factors, including the mitogen-activated protein kinase (MAPK) superfamily. MAPK phosphatase 3 (MKP-3) is a cytoplasmic dual-specificity phosphatase specific for extracellular signal-regulated kinase 1/2 (Erk1/2). Recent evidence indicates that hypoxia increases the endogenous levels of both MKP-3 mRNA and protein. However, its role in the response of cells to hypoxia is poorly understood. Herein, we demonstrated that small-interfering RNA (siRNA)-mediated knockdown of MKP-3 enhanced HIF-1α (not HIF-2α) levels. Conversely, MKP-3 overexpression suppressed HIF-1α (not HIF-2α) levels, as well as the expression levels of hypoxia-responsive genes (LDHA, CA9, GLUT-1, and VEGF), in hypoxic colon cancer cells. These findings indicated that MKP-3, induced by HIF-1α in hypoxia, negatively regulates HIF-1α protein levels and hypoxia-responsive genes. However, we also found that long-term hypoxia (>12 h) induced proteasomal degradation of MKP-3 in a lactic acid-dependent manner. Taken together, MKP-3 expression is modulated by the hypoxic conditions prevailing in colon cancer, and plays a role in cellular adaptation to tumor hypoxia and tumor progression. Thus, MKP-3 may serve as a potential therapeutic target for colon cancer treatment.

• Journal of Korean Neurosurgical Society
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• v.46 no.4
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• pp.389-396
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• 2009

Objective : Triptolide (TP) has been reported to suppress the expression of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1), of which main function is to inactivate the extracellular signal-regulated kinase-1/2 (ERK-1/2), the p38 MAPK and the c-Jun N-terminal kinase-1/2 (JNK-1/2), and to exert antiproliferative and pro-apoptotic activities. However, the mechanisms underlying antiproliferative and pro-apoptotic activities of TP are not fully understood. The purpose of this study was to examine whether the down-regulation of MKP-1 expression by TP would account for antiproliferative activity of TP in immortalized HT22 hippocampal cells. Methods : MKP-1 expression and MAPK phosphorylation were analyzed by Western blot. Cell proliferation was assessed by $^3H$-thymidine incorporation. Small interfering RNA (siRNA) against MKP-1, vanadate (a phosphatase inhibitor), U0126 (a specific inhibitor for ERK-1/2), SB203580 (a specific inhibitor for p38 MAPK), and SP600125 (a specific inhibitor for JNK-1/2) were employed to evaluate a possible mechanism of antiproliferative action of TP. Results : At its non-cytotoxic dose, TP suppressed MKP-1 expression, reduced cell growth, and induced persistent ERK-1/2 activation. Similar growth inhibition and ERK-1/2 activation were observed when MKP-1 expression was blocked by MKP-1 siRNA and its activity was inhibited by vanadate. The antiproliferative effects of TP, MKP-1 siRNA, and vanadate were significantly abolished by U0126, but not by SB203580 or SP600125. Conclusion : Our findings suggest that TP inhibits the growth of immortalized HT22 hippocampal cells via persistent ERK-1/2 activation by suppressing MKP-1 expression. Additionally, this study provides evidence supporting that MKP-1 may play an important role in regulation of neuronal cell growth.

• Journal of Soil and Groundwater Environment
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• v.20 no.6
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• pp.28-36
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• 2015

Simultaneous mobility reduction of explosives and heavy metals in an operational range by monopotassium phosphate (MKP) and bentonite spreading technology was investigated. Potassium ion and phosphate ion in MKP act as explosives sorption enhancer and insoluble heavy metal phosphate formation, respectively, while bentonite acts as the explosives adsorbent. Then, the decrease in surface water concentration of the pollutants and resulting risk reduction for local residents of the operational range, by MKP/bentonite application was estimated. Under untreated scenario, the noncancer hazard index (HI) exceeded unity on February, July and August, mainly due to 2,4,6-trinitrotoluene (TNT); however, MKP/bentonite treatment was expected to lower the noncancer hazard index by decreasing the surface water concentration of explosives and heavy metals (especially TNT). For example, on July, estimated surface water concentration and HI of TNT were 0.01 mg/L and 1.1, respectively, meanwhile the sorption coefficient of TNT was 3.9 mg¹⁻ⁿkg⁻¹Lⁿ. However, by MKP/bentonite treatment, the TNT sorption coefficient increased to 113.8 mg¹⁻ⁿkg⁻¹Lⁿ and the surface water concentration and HI decreased to about 0.002 mg/L and 0.2, respectively. Based on the result, it can be concluded that MKP/bentonite spreading is a benign technology that can mitigate the risk posed by the pollutants migration from operational ranges.

• BMB Reports
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• v.47 no.12
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• pp.685-690
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• 2014

The Ras/Raf/MEK/Erk signaling pathway is important for regulation of cell growth, proliferation, differentiation, survival, and apoptosis in response to a variety of extracellular stimuli. Lack of Erk MAPK activation is observed in several cancer cells despite active activation of Ras. However, little is known about the modulation of Erk1/2 activity by active Ras. Here, we show that overexpression of active H-Ras (H-RasG12R) in NIH3T3 fibroblasts impaired FGF2-induced Erk1/2 phosphorylation, as compared to wild-type cells. Northern blot analysis revealed that prolonged expression of active Ras increased MAP kinase phosphatase 3 (MKP3) mRNA expression, a negative regulator of Erk MAPK. Inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway abrogated active Ras-induced up-regulation of MKP3 expression, leading to the rescue of Erk1/2 phosphorylation. Our results demonstrated that the Ras/Raf/MEK/Erk signaling cascade is negatively regulated by the PI3K/Aktdependent transcriptional activation of the MKP3 gene.

• IMMUNE NETWORK
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• v.16 no.2
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• pp.85-98
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• 2016

The mitogen-activated protein kinases (MAPKs) are key regulators of cell growth and survival in physiological and pathological processes. Aberrant MAPK signaling plays a critical role in the development and progression of human cancer, as well as in determining responses to cancer treatment. The MAPK phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are a family of proteins that function as major negative regulators of MAPK activities in mammalian cells. Studies using mice deficient in specific MKPs including MKP1/DUSP1, PAC-1/DUSP2, MKP2/DUSP4, MKP5/DUSP10 and MKP7/DUSP16 demonstrated that these molecules are important not only for both innate and adaptive immune responses, but also for metabolic homeostasis. In addition, the consequences of the gain or loss of function of the MKPs in normal and malignant tissues have highlighted the importance of these phosphatases in the pathogenesis of cancers. The involvement of the MKPs in resistance to cancer therapy has also gained prominence, making the MKPs a potential target for anti-cancer therapy. This review will summarize the current knowledge of the MKPs in cancer development, progression and treatment outcomes.

• Journal of Soil and Groundwater Environment
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• v.23 no.6
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• pp.46-53
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• 2018

Mobility reduction of 2,4,6-trinitrotoluene (TNT) was tested by amending monopotassium phosphate (MKP) and montmorillonite to a firing range soil contaminated with TNT. While addition of MKP enhanced sorption of TNT on soil matrix, and combined use of MKP with montmorillonite significantly decreased desorption of TNT as well as remarkably increased the TNT sorption. Montmorillonite amendment by 5% of soil mass resulted in TNT desorption of 0.12 mg/kg from soil loaded with 9.93 mg/kg-TNT. The decrease of TNT desorption was proportional to the amount of montmorillonite amended. At 10 and 15% amendment, only 0.79 and 1.23 mg/kg-TNT was desorbed from 29.33 and 48.80 mg/kg-TNT. In addition, the leaching of TNT with synthetic precipitation leaching procedure (SPLP) and hydroxypropyl-${\beta}$-cyclodextrin (HPCD) decreased, indicating that TNT in MKP/montmorillonite-treated soil became more stable and less leachable. The results demonstrate that addition of MKP and montmorillonite to TNT-contaminated soil reduces the mobility of TNT from soil not only by increasing TNT sorption, but also decreasing TNT desorption. It was found that MKP and montmorillonite amendments by 5 and 10% of soil mass, respectively, were optimal for reducing the mobility of soil TNT.

• Biomedical Science Letters
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• v.27 no.4
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• pp.223-230
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• 2021

Tumor necrosis factor alpha (TNF-α) is a principal regulator of inflammation and immunity. The proinflammatory properties of TNF-α can be attributed to its ability to activate the enzyme cytosolic phospholipase A₂ (cPLA₂), which generates potent inflammatory lipid mediators, eicosanoids. L-glutamine (Gln) plays physiologically important roles in various metabolic processes. We have reported that Gln has a potent anti-inflammatory activity via rapid upregulation of mitogen-activated protein kinases (MAPKs) phosphatase (MKP)-1, which preferentially dephosphorylates the key proinflammatory enzymes, p38 MAPK and cytosolic phospholipase A₂ (cPLA₂). In this study, we have investigated whether Gln could inhibit TNF-α-induced cPLA₂ activation. Gln inhibited TNF-α-induced increases in cPLA₂ phosphorylation in the lungs and blood levels of the cPLA₂ metabolites, leukotrine B4 (LTB4) (lipoxygenase metabolite) and prostaglandin E2 (PGE2) (cyclooxygenase metabolite). TNF-α increased p38 and cPLA₂ phosphorylation and blood levels of LTB4 and PGE2, which were blocked by the p38 inhibitor SB202190. Gln inhibited TNF-α-induced p38 and cPLA₂ phosphorylation and production of the cPLA₂ metabolites. Such inhibitory activity of Gln was no longer observed in MKP-1 small interfering RNA-pretreated animals. Our data indicate that Gln inhibited TNF-α-induced cPLA₂ phosphorylation through MKP-1 induction/p38 inhibition, and suggest that the utility of Gln in inflammatory diseases in which TNF-α plays a major role in their pathogenesis.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.53 no.4
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• pp.606-619
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• 2020

This study investigated the effects of crude protein levels in diets containing monobasic potassium phosphate (MKP) on water quality and the growth of Japanese eels Anguilla japonica and leafy vegetables in a Hybrid BFT-Aquaponics (HBFT-AP) system. The first experiment (EXP1) was designed to verify the effects of the feed itself on leafy vegetable productivity using two diets (CP48 and CP30) with MKP and one commercial eel diet (COM58). The second experiment (EXP2) examined the effects of the three diets on productivity of the fish and leafy vegetables in the HBFT-AP for 6 weeks. After the 6 week feeding trial, the weight gain, feed efficiency, specific growth rate and protein efficiency ratio of fish fed COM58 and CP48 were higher than those of fish fed CP30 (P<0.05) and the growth of the four leafy vegetables was the highest with fish fed CP48. Water quality was measured six times per week using a portable water quality meter and reagent measurements and showed variance with time for TAN (0.01-0.09 mg/L), NO₂-N (0.010-0.064 mg/L), NO₃-N (5.52-27.15 mg/L), PO₄-P (2.03-5.32 mg/L) and pH (7.86-6.15).