• 제목/요약/키워드: Growth-inhibitor

검색결과 1,018건 처리시간 0.03초

Antagonistic Regulation of Arabidopsis Growth by Brassinosteroids and Abiotic Stresses

  • Chung, Yuhee;Kwon, Soon Il;Choe, Sunghwa
    • Molecules and Cells
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    • 제37권11호
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    • pp.795-803
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    • 2014
  • To withstand ever-changing environmental stresses, plants are equipped with phytohormone-mediated stress resistance mechanisms. Salt stress triggers abscisic acid (ABA) signaling, which enhances stress tolerance at the expense of growth. ABA is thought to inhibit the action of growth-promoting hormones, including brassinosteroids (BRs). However, the regulatory mechanisms that coordinate ABA and BR activity remain to be discovered. We noticed that ABA-treated seedlings exhibited small, round leaves and short roots, a phenotype that is characteristic of the BR signaling mutant, brassinosteroid insensitive1-9 (bri1-9). To identify genes that are antagonistically regulated by ABA and BRs, we examined published Arabidopsis microarray data sets. Of the list of genes identified, those upregulated by ABA but downregulated by BRs were enriched with a BRRE motif in their promoter sequences. After validating the microarray data using quantitative RT-PCR, we focused on RD26, which is induced by salt stress. Histochemical analysis of transgenic Arabidopsis plants expressing RD26pro:GUS revealed that the induction of GUS expression after NaCl treatment was suppressed by co-treatment with BRs, but enhanced by co-treatment with propiconazole, a BR biosynthetic inhibitor. Similarly, treatment with bikinin, an inhibitor of BIN2 kinase, not only inhibited RD26 expression, but also reduced the survival rate of the plant following exposure to salt stress. Our results suggest that ABA and BRs act antagonistically on their target genes at or after the BIN2 step in BR signaling pathways, and suggest a mechanism by which plants fine-tune their growth, particularly when stress responses and growth compete for resources.

Growth inhibition and cell cycle phase-specific apoptosis induced by celecoxib in human NSCLC cells in vitro.

  • Choi, Kang-Eun;Kang, Jin-Hyoung;Kuh, Hyo-Jeong
    • 대한약학회:학술대회논문집
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    • 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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    • pp.244.1-244.1
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    • 2002
  • Cyclooxygenase-2 ( COX-2 ) is an inducible enzyme which produces prostanoids by various stimuli. Overexpression of COX-2 in many tumor types indicates its association with tumor progression, which has been a promising target for chemoprevention and chemomodulation. We studied conc- and time-dependency of COX-2 inhibition, growth inhibition, and cell cycle arrest induced by celecoxib, a selective COX-2 inhibitor, in human non-small cell lung cancer (NSCLC) A549 cells. (omitted)

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Heat shock protein 90 inhibitor AUY922 attenuates platelet-derived growth factor-BB-induced migration and proliferation of vascular smooth muscle cells

  • Kim, Jisu;Lee, Kang Pa;Kim, Bom Sahn;Lee, Sang Ju;Moon, Byung Seok;Baek, Suji
    • The Korean Journal of Physiology and Pharmacology
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    • 제24권3호
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    • pp.241-248
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    • 2020
  • Luminespib (AUY922), a heat shock proteins 90 inhibitor, has anti-neoplastic and antitumor effects. However, it is not clear whether AUY922 affects events in vascular diseases. We investigated the effects of AUY922 on the platelet-derived growth factor (PDGF)-BB-stimulated proliferation and migration of vascular smooth muscle cells (VSMC). VSMC viability was detected using the XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) reagent. To detect the attenuating effects of AUY922 on PDGF-BB-induced VSMCs migration in vitro, we performed the Boyden chamber and scratch wound healing assays. To identify AUY922-mediated changes in the signaling pathway, the phosphorylation of protein kinase B (Akt) and extracellular signal-regulated kinase (ERK) 1/2 was analyzed by immunoblotting. The inhibitory effects of AUY922 on migration and proliferation ex vivo were tested using an aortic ring assay. AUY922 was not cytotoxic at concentrations up to 5 nM. PDGF-BB-induced VSMC proliferation, migration, and sprout outgrowth were significantly decreased by AUY922 in a dose-dependent manner. AUY922 significantly reduced the PDGF-BB-stimulated phosphorylation of Akt and ERK1/2. Furthermore, PD98059 (a selective ERK1/2 inhibitor) and LY294002 (a selective Akt inhibitor) decreased VSMC migration and proliferation by inhibiting phosphorylation of Akt and ERK1/2. Greater attenuation of PDGF-BB-induced cell viability and migration was observed upon treatment with PD98059 or LY294002 in combination with AUY922. AUY922 showed anti-proliferation and anti-migration effects towards PDGF-BB-induced VSMCs by regulating the phosphorylation of ERK1/2 and Akt. Thus, AUY922 is a candidate for the treatment of atherosclerosis and restenosis.

Effects of gintonin on the proliferation, migration, and tube formation of human umbilical-vein endothelial cells: involvement of lysophosphatidic-acid receptors and vascular-endothelial-growth-factor signaling

  • Hwang, Sung-Hee;Lee, Byung-Hwan;Choi, Sun-Hye;Kim, Hyeon-Joong;Won, Kyung Jong;Lee, Hwan Myung;Rhim, Hyewon;Kim, Hyoung-Chun;Nah, Seung-Yeol
    • Journal of Ginseng Research
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    • 제40권4호
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    • pp.325-333
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    • 2016
  • Background: Ginseng extracts are known to have angiogenic effects. However, to date, only limited information is available on the molecular mechanism underlying the angiogenic effects and the main components of ginseng that exert these effects. Human umbilical-vein endothelial cells (HUVECs) are used as an in vitro model for screening therapeutic agents that promote angiogenesis and wound healing. We recently isolated gintonin, a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand, from ginseng. LPA plays a key role in angiogenesis and wound healing. Methods: In the present study, we investigated the in vitro effects of gintonin on proliferation, migration, and tube formation of HUVECs, which express endogenous LPA1/3 receptors. Results: Gintonin stimulated proliferation and migration of HUVECs. The LPA1/3 receptor antagonist, Ki16425, short interfering RNA against LPA1 or LPA3 receptor, and the Rho kinase inhibitor, Y-27632, significantly decreased the gintonin-induced proliferation, migration, and tube formation of HUVECs, which indicates the involvement of LPA receptors and Rho kinase activation. Further, gintonin increased the release of vascular endothelial growth factors from HUVECs. The cyclooxygenase-2 inhibitor NS-398, nuclear factor kappa B inhibitor BAY11-7085, and c-Jun N-terminal kinase inhibitor SP600125 blocked the gintonin-induced migration, which shows the involvement of cyclooxygenase-2, nuclear factor kappa B, and c-Jun N-terminal kinase signaling. Conclusion: The gintonin-mediated proliferation, migration, and vascular-endothelial-growth-factor release in HUVECs via LPA-receptor activation may be one of in vitro mechanisms underlying ginsenginduced angiogenic and wound-healing effects.

Malassezia pachydermatis에 의한 세포 내 Tyrosinase 저해제의 생산 (Production of Intracelluar Tyrosinase Inhibitor from Malassezia pachydermatis)

  • 이성현;유형은;곽윤진;김효진;이대형;이종수
    • 자연과학논문집
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    • 제14권2호
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    • pp.93-102
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    • 2004
  • A yeast strain SL-27 found to produce active intracellular tyrosinase inhibitor was screened from 972 kinds of yeasts. It was identified as Malassezia pachydermatis based on microbiological characteristics. The optimum pH and temperature for the growth of Malassezia pachydermatis SL-27 were pH 7.0 and $37^{\circ}C$, respectively. The optimal culture conditions for the production of tyrosinase inhibitor by Malassezia pachydermatis SL-27 were investigated. The optimal medium cimposition for tyrosinase inhibitor production was determined to be 1.0% casamino acid, 2.0% glucose, 0.1% $KH_2PO_4$, 0.05% $MgSo_{4-}7H20$ and each 0.01 of $CaCl_2$ and NaCl. Optimal initial pH and temperature for the production of tyrosinase inhibitor were pH 5.0 and $30^{\circ}C$, respectively. The maximum tyrosinase inhibitory activity of 84%/mL of cell-free extract was showed after 12 h of cultivation under the optimal culturing conditions.

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Anti-invasive activity of histone deacetylase inhibitors via the induction of Egr-1 and the modulation of tight junction-related proteins in human hepatocarcinoma cells

  • Kim, Sung-Ok;Choi, Byung-Tae;Choi, Il-Whan;Cheong, Jae-Hun;Kim, Gi-Young;Kwon, Taeg-Kyu;Kim, Nam-Deuk;Choi, Yung-Hyun
    • BMB Reports
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    • 제42권10호
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    • pp.655-660
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    • 2009
  • The potential anti-metastasis and anti-invasion activities of early growth response gene-1 (Egr-1) and claudin-3, a tight junction (TJ)-related protein, were evaluated using histone deacetylase (HDAC) inhibitors in human hepatocarcinoma cells. The results of wound healing and Transwell assays showed that HDAC inhibitors such as trichostatin A and sodium butyrate inhibited cell migration and invasion. HDAC inhibitors markedly induced Egr-1 expression during the early period, after which expression levels decreased. In addition, the down-regulation of snail and type 1 insulin-like growth factor receptor (IGF-1R) in HDAC inhibitor- treated cells induced the upregulation of thrombospondin-1 (TSP-1), E-cadherin and claudin-3. Cells transfected with Egr-1 and claudin-3 siRNA displayed significant blockage of HDAC inhibitor-induced anti-invasive activity. Collectively, these findings indicate that the up-regulation of Egr-1 and claudin-3 are crucial steps in HDAC inhibitor-induced anti-metastasis and anti-invasion.

곤충의 식물병원성 진균에 대한 항균활성 (Antifungal Activities of Insect Against the Plant Pathogenic Fungi)

  • 김경아;이경렬;송경식;노시갑
    • 한국잠사곤충학회지
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    • 제48권2호
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    • pp.68-72
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    • 2006
  • 본 연구는 식물병원성곰팡이에 대한 곤충 혈액 및 유충체의 항곰팡이 활성을 조사하였다. 집누에, 장수풍뎅이, 흰점박이 꽃무지 모두 곰팡이 저해활성을 나타냈으며, 집누에의 계통간 비교에서는 1087계통의 활성이 가장 높았다. 또한, 혈액보다는 유충체를 이용한 경우가 더 강한 항곰팡이 활성을 나타냈다. 곤충의 항곰팡이 활성은 곰팡이균주에 따라 다르며, 본 연구에 사용된 3종은 A. panax, C. gloeosporioides 및 P. oryzae 균에 항곰팡이 활성을 가진다.