• Title/Summary/Keyword: Upregulation

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Comparisons between White Ginseng Radix and Rootlet for Antidiabetic Activity and Mechanism in KKAy Mice

  • Chung, Sung-Hyun;Choi, Chang-Geun;Park, Se-Ho
    • Archives of Pharmacal Research
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    • v.24 no.3
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    • pp.214-218
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    • 2001
  • The mechanisms responsible for the antidiabetic activity of both the white ginseng radix (Ginseng Radix Alba, GRA) and the rootlet (Cinseng Radix Palva, GRP) were investigated. After a four week oral administration, the fasting blood glucose levels in the GRA- and GRP-treated groups were lower when compared to the control group. To elucidate the hypoglycemic mechanism(s) of the ginseng radices, glucose absorption from the small intestine, hepatic hexokinase and glucose-6-phosphatase activities, in addition to PPAR-${\gamma}$ expression in adipose tissue were examined. The results strongly suggest that GRA can improve hyperglycemia in KKAy mice, possibly by blocking intestinal glucose absorption and inhibiting hepatic glucose-6-phosphatase, and GRP through the upregulation of adipocytic PPAR-$\gamma$ protein expression as well as inhibiting intestinal glucose absorption.

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Cellular Changes Resulting from Forced Expression of Glypican-3 in Hepatocellular Carcinoma Cells

  • Kwack, Mi Hee;Choi, Byung Yeol;Sung, Young Kwan
    • Molecules and Cells
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    • v.21 no.2
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    • pp.224-228
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    • 2006
  • Glypican-3 (GPC3) is a member of the glypican family, which encodes cell-surface heparan-sulfate proteoglycans, and is frequently upregulated in hepatocellular carcinoma (HCC). We have recently reported that blocking endogenous GPC3 expression promotes the growth of HCC cell lines, suggesting that GPC3 plays a negative role in HCC cell proliferation. Here, we report that forced expression of GPC3 reduced the growth of HCC cells. We also found that FGF2-mediated cell proliferation was inhibited by GPC3. In addition, we observed that the adhesion of HCC cells to collagen type I and fibronectin was decreased by GPC3, whereas cellular migration and invasiveness were stimulated. Collectively, these results suggest that progression of hepatocellular carcinoma is associated with upregulation of GPC3.

Oxidative DNA damage and its repair enzyme expression induced by welding fume inhalation.

  • Kim, Soo-Jin;Paik, Sang-Gi;Yu, Il-Je;Oky Maeng;Hyun, Jin-Suk;Sung, Jae-Hyuk;Han, Jeong-Hee;Maeng, Seung-Hee
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2003.10b
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    • pp.126-126
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    • 2003
  • Welding fume (WF) induces pulmonary disease including pneumoconiosis. To investigate whether reactive oxygen species-induced oxidative DNA damage occurs during welding fume exposure and the upregulation of DNA repair mechanisms is accompanied, SPF SD rats were exposed to welding fumes with the concentrations of 65.6${\pm}$2.9 mg/㎥(low dose) and 116.8${\pm}$3.9 mg/㎥ (high dose) of total suspended particulate for 2 hrs per day in an inhalation chamber for a total of 2hrs, 15 or 30 days.(omitted)

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Oncogenic RUNX3: A Link between p53 Deficiency and MYC Dysregulation

  • Date, Yuki;Ito, Kosei
    • Molecules and Cells
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    • v.43 no.2
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    • pp.176-181
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    • 2020
  • The RUNX transcription factors serve as master regulators of development and are frequently dysregulated in human cancers. Among the three family members, RUNX3 is the least studied, and has long been considered to be a tumor-suppressor gene in human cancers. This idea is mainly based on the observation that RUNX3 is inactivated by genetic/epigenetic alterations or protein mislocalization during the initiation of tumorigenesis. Recently, this paradigm has been challenged, as several lines of evidence have shown that RUNX3 is upregulated over the course of tumor development. Resolving this paradox and understanding how a single gene can exhibit both oncogenic and tumor-suppressive properties is essential for successful drug targeting of RUNX. We propose a simple explanation for the duality of RUNX3: p53 status. In this model, p53 deficiency causes RUNX3 to become an oncogene, resulting in aberrant upregulation of MYC.

Upregulation of Endosymbiont Densities in Bemisia tabaci by Acquisition of Tomato Yellow Leaf Curl Virus

  • Jahan, S.M. Hemayet;Lee, Kyeong-Yeoll
    • Current Research on Agriculture and Life Sciences
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    • v.30 no.2
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    • pp.124-130
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    • 2012
  • Sweetpotato whitefly, Bemisia tabaci, is a vector of more than 100 plant-diseased viruses, as well as a serious pest of various horticultural plants. This species harbors a primary endosymbiont Portiera along with several secondary endosymbionts such as Cardinium and Hamiltonella. We investigated whether or not TYLCV acquisition alters the densities of endosymbionts in the body of B. tabaci using quantitative real-time PCR. Our results showed that the densities of both Cardinium and Hamiltonella, but not Portiera, increased upon acquisition of TYLCV. In addition, expression of GroEL, a molecular chaperone produced by Hamiltonella, was significantly upregulated in TYLCV-infected whiteflies. Our results suggest that endosymbionts may play an important role in TYLCV transmission mechanism within the body of B. tabaci.

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The Effect of allicin on radiation-induced expression of ICAM-l and of activation of JNK and p38 MAP kinase pathway in human endothelial cells.

  • Mo, Sung-Ji;Son, Eun-Hwa;Cho, Seong-Jun;Yang, Kwang-Hee;Rhee, Dong-Kwon;Pyo, Suhk-Neung
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.130.3-131
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    • 2003
  • Inflammation is a frequent radiation-induced following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. We examined the effect if allicin, a major component of garlic, on the induction of intercellular adhesion molecule-l (ICAM-1) by gamma-irradiation and the mechanisms of its effect in gamma-irradiated human umbilical vein endothelial cells (HUVECs). (omitted)

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15-DEoxy-$d^{12,14}$ Prostaglandin $J_2$ Rescues Pc12 Cells From Hydrogen Peroxide-induced Apoptosis Through Upregulation Of Heme Oxygenase-1

  • Kim, Ji-Woo;Jang, Jung-Hee;Surh, Young-Joon
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.153.1-153.1
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    • 2003
  • Oxidative stress induced by reactive oxygen intermediates (ROIs) has been implicated in a variety of human diseases including cancer, diabetes, rheumatoid arthritis and neurodegenerative disorders. Hydrogen peroxide ($H_2O_2$), a representative ROI which is produced during the cellular redox process, can cause cell death via apoptosis and/or necrosis depending on its concentrations. l5-Deoxy-$D^{12, 14}$ prostaglandin $J_2$ (15d-$PGJ_2$), a dehydration product of prostaglandin $D_2$, has been reportd to possess a number of biological activities such as anti-inflammatory, anticarcinogenic, and antioxidative properties. (omitted)

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Induction of apoptosis in human pro myelocytic leukaemia HL-60 cells by manassatin B involves release of cytochrome c and activation of caspases

  • Seo , bo-Rim;Lee, kyung-Tae
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.316.2-316.2
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    • 2002
  • Manassantin B classified into dineolignans have been isolated from Saururus chinensis Manassantin B was found to induce apoptosis in human promyelocytic leukaemia HL -60 cells with characteristic apoptotic features like increase of nucleosomalladder. apoptotic body ormation. flipping of membrane phosphatidylserine. Manassantin B induced FAS and FAS ligand expression, and activated caspase 8 which cleaved bid to tbid in cytosol. The release of cytochrome c to sytosol was accompanied with decrease of bcl-2 protein and incresase of tbid and bax protein in mitochondria. Released xytochrome c activated caspase 9 and-3. but these effects were completely attenuated by the treatment of broad caspses ingibitor. Z-VAD fmk. These results indicate that manassatin B induce apoptosis through upregulation of FAS. caspase family and mitochondria-related proteins.

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Allicin reduces expression of Intercellular Adhesion Molecule-1 (ICAM-1) in gamma-irradiated endothelial cells: Involvement of p38 MAP kinase signalling pathway.

  • Son, Eun-Hwa;Mo, Sung-Ji;Cho, Seong-Jun;Yang, Kwang-Hee;Rhee, Dong-Kwon;Pyo, Suhk-Neung
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.307.1-307.1
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    • 2002
  • Inflammation is a frequent radiation-induced following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface has been known to be associated with inflammation. interfering with the expression of adhesion molecules is an important therapeutic target. We examined the effect of allicin. a major component of garlic. on the induction of intercellular adhesion molecule-1 (lCAM-1) by gamma-irradiation and the mechanisms of its effect in gamma-irradiated human umbilical vein endothelial cells (HUVECs). (omitted)

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Autophagy down-regulates NLRP3-dependent inflammatory response of intestinal epithelial cells under nutrient deprivation

  • Yun, Yewon;Baek, Ahruem;Kim, Dong-Eun
    • BMB Reports
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    • v.54 no.5
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    • pp.260-265
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    • 2021
  • Dysregulation of inflammation induced by noninfectious stress conditions, such as nutrient deprivation, causes tissue damage and intestinal permeability, resulting in the development of inflammatory bowel diseases. We studied the effect of autophagy on cytokine secretion related to intestinal permeability under nutrient deprivation. Autophagy removes NLRP3 inflammasomes via ubiquitin-mediated degradation under starvation. When autophagy was inhibited, starvation-induced NLRP3 inflammasomes and their product, IL-1β, were significantly enhanced. A prolonged nutrient deprivation resulted in an increased epithelial mesenchymal transition (EMT), leading to intestinal permeability. Under nutrient deprivation, IL-17E/25, which is secreted by IL-1β, demolished the intestinal epithelial barrier. Our results suggest that an upregulation of autophagy maintains the intestinal barrier by suppressing the activation of NLRP3 inflammasomes and the release of their products, including pro-inflammatory cytokines IL-1β and IL-17E/25, under nutrient deprivation.