• 제목/요약/키워드: Event Activation

검색결과 143건 처리시간 0.034초

홍삼수용성추출물이 혈관신생에 미치는 영향 (Angiogenic Effects of Korea Red Ginseng Water Extract in the In Vitro and In Vivo Models)

  • 노의준;유승훈;김규민;이상현;윤용갑
    • 동의생리병리학회지
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    • 제23권2호
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    • pp.416-425
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    • 2009
  • Angiogenesis is important for promoting cardiovascular disease, wound healing, and tissue regeneration. We here investigated the pharmacological effects of Korea red ginseng water extract (KRGE) on angiogenesis and its underlying signal mechanism. This study showed that KRGE increased in vitro proliferation, migration, and tube formation of human umbilical endothelial cells, as well as stimulated in vivo angiogenesis. KRGE-induced angiogenesis was accompanied by phosphorylation of ERK1/2, Akt, and endothelial nitric oxide synthase (eNOS) as well as an increase in NO production. Inhibition of PI3K activity by wortmannin completely inhibited KRGE-induced angiogenesis and phosphorylation of Akt, ERK1/2, and eNOS, indicating that PI3K/Akt activation is an upstream event of KRGE-mediated angiogenic pathway. The MEK inhibitor PD98059 completely blocked KRGE-induced angiogenesis and ERK phosphorylation without affecting Akt and eNOS activation. However, the eNOS inhibitor NMA effectively inhibited tube formation, but partially blocked proliferation and migration as well as ERK phosphorylation without altering Akt and eNOS activation, revealing that eNOS/NO pathway is in part involved in ERK1/2 activation. This study first demonstrated the critical involvement of both ERK1/2 and eNOS activation in KRGE-induced angiogenesis, which lie on downstream of PI3K/Akt. Thus, these results indicate that KRGE requires activation of both the PI3K/Akt-dependent ERK1/2 and eNOS signal pathways and their cross-talk for its full angiogenic activity.

호텔 레스토랑 프로모션 메뉴의 환경요인이 영업활성화 전략에 미치는 영향 (Plan to Improve Business in Hotel's Restaurant by Promotional Menu of Circumstance Factor)

  • 전진화;배인호
    • 한국조리학회지
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    • 제13권1호
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    • pp.192-203
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    • 2007
  • The purpose of this study is to figure out the plans to improve business in Hotel French restaurants. This study conducts documentary study and empirical study. To achieve the purpose, a survey was conducted by 172 staffs of Hotel French restaurants in Seoul. The result of this research is as follows. Hotel restaurant operators recognize the importance of promotion and development of new sales goods. But they haven't done long-term marketing directions focusing on cost-saving and ephemeral sales promotion effects. Hotel restaurants should establish public information strategies uniformly and look for the plans that offer customers adequate information. Also, they should make a differentiation strategy within the same industry, can always give recency to customers, and enhance the event-connecting promotion menu and business activation.

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Inhibition of Homodimerization of Toll-like Receptor 4 by 6-Shogaol

  • Ahn, Sang-Il;Lee, Jun-Kyung;Youn, Hyung-Sun
    • Molecules and Cells
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    • 제27권2호
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    • pp.211-215
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    • 2009
  • Toll-like receptors (TLRs) play a critical role in sensing microbial components and inducing innate immune and inflammatory responses by recognizing invading microbial pathogens. Lipopolysaccharide-induced dimerization of TLR4 is required for the activation of downstream signaling pathways including nuclear factor-kappa B ($NF-{\kappa}B$). Therefore, TLR4 dimerization may be an early regulatory event in activating ligand-induced signaling pathways and induction of subsequent immune responses. Here, we report biochemical evidence that 6-shogaol, the most bioactive component of ginger, inhibits lipopolysaccharide-induced dimerization of TLR4 resulting in the inhibition of $NF-{\kappa}B$ activation and the expression of cyclooxygenase-2. Furthermore, we demonstrate that 6-shogaol can directly inhibit TLR-mediated signaling pathways at the receptor level. These results suggest that 6-shogaol can modulate TLR-mediated inflammatory responses, which may influence the risk of chronic inflammatory diseases.

Radiation-induced Tumorigenesis

  • Kim, In-Gyu;Lee, Yun-Sil
    • BMB Reports
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    • 제36권1호
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    • pp.144-148
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    • 2003
  • During the past 2 decades, radiation tumorigenesis researchers have focused on cellular and molecular mechanisms. We reviewed some of these research fields, since they may specifically relate to the induction of cancer by ionizing radiation. First, radiation-mediated mutation was discussed. Then the initiating event in radiation carcinogenesis, as well as other genetic events that may by involved, is discussed in terms of the possible role of the activation of genes and the loss of cell-cycle checkpoints.

이중언어환경에서의 언어간 부호전환 수준에 따른 차별적 신경활성화 과정: ERP연구 (Differential Effect for Neural Activation Processes according to the Proficiency Level of Code Switching: An ERP Study)

  • 김충명
    • 말소리와 음성과학
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    • 제2권4호
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    • pp.3-10
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    • 2010
  • The present study aims to investigate neural activations according to the level of code switching in English proficient bilinguals and to find the relationship between the performance of language switching and proficiency level using ERPs (event-related potentials). First, when comparing high-proficient (HP) with low-proficient (LP) bilingual performance in a native language environment, the activation level of N2 was observed to be higher in the HP group than in the LP group, but only under two conditions: 1) the language switching (between-language) condition known as indexing attention of code switching and 2) the inhibition of current language for L1. Another effect of N400 can be shown in both groups only in the language non-switching (within-language) condition. This effect suggests that both groups completed the semantic acceptability task well in their native language environment without the burden of language switching, irrespective of high or low performance. The latencies of N400 are only about 100ms earlier in the HP group than in the LP group. This difference can be interpreted as facilitation of the given task. These results suggest that HP showed the differential activation in inhibitory system for L1 in switching condition of L1-to-L2 to be contrary to inactivation of inhibitory system for the LP group. Despite the absence of an N400 effect at the given task in both groups, differential latencies between the peaks were attributed to the differences of efficiency in semantic processing.

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학교도서관의 북큐레이션 활성화 방안에 대한 탐색적 연구 - 인천 중등 학교도서관 사례 및 현황 분석을 중심으로 - (An Exploratory Study on the Activation of Book Curation in School Libraries: Focused on the Case and Current Status Analysis of Secondary School Library in Incheon)

  • 오혜민 ;곽승진
    • 한국비블리아학회지
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    • 제33권4호
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    • pp.115-137
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    • 2022
  • 본 연구는 중등 학교도서관 북큐레이션 사례 조사와 담당자의 북큐레이션에 대한 인식 분석을 통해 중등 학교도서관 북큐레이션 활성화 방안을 제시하는 데 목적이 있다. 문헌조사와 함께, 인천광역시교육청 중등 학교 중 상시 운영이 이루어지는 전수 192개 학교도서관 담당자를 대상으로 설문조사, 인천 중등 사서교사 4명과 문헌정보학과 교수 1명을 대상으로 인터뷰, 학교도서관 방문 관찰을 병행하였다. 이를 통해 북큐레이션 활성화 방안으로 학교도서관 담당자의 증원, 교과교사와의 협력과 정보 공유, 북큐레이션 운영을 위한 매뉴얼 확립, 주제 선정 사례집 출판을 제안하였다.

p38 MAPK Signaling Mediates Mitochondrial Apoptosis in Cancer Cells Induced by Oleanolic Acid

  • Liu, Jia;Wu, Ning;Ma, Lei-Na;Zhong, Jia-Teng;Liu, Ge;Zheng, Lan-Hong;Lin, Xiu-Kun
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권11호
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    • pp.4519-4525
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    • 2014
  • Oleanolic acid (OA) is a nutritional component widely distributed in various vegetables. Although it has been well recognized for decades that OA exerts certain anti-tumor activity by inducing mitochondria-dependent apoptosis, it is still unclear that what molecular signaling is responsible for this effect. In this study, we employed cancer cell lines, A549, BXPC-3, PANC-1 and U2OS to elucidate the molecular mechanisms underlying OA anti-tumor activity. We found that activation of MAPK pathways, including p-38 MAPK, JNK and ERK, was triggered by OA in both a dose and time-dependent fashion in all the tested cancer cells. Activation was accompanied by cleavage of caspases and PARP as well as cytochrome C release. SB203580 (p38 MAPK inhibitor), but not SP600125 (JNK inhibitor) and U0126 (ERK inhibitor), rescued the pro-apoptotic effect of OA on A549 and BXPC-3 cells. OA induced p38 MAPK activation promoted mitochondrial translocation of Bax and Bim, and inhibited Bcl-2 function by enhancing their phosphorylation. OA can induce reactive oxygen species (ROS)-dependent ASK1 activation, and this event was indispensable for p38 MAPK-dependent apoptosis in cancer cells. In vivo, p38 MAPK knockdown A549 tumors proved resistant to the growth-inhibitory effect of OA. Collectively, we elucidated that activation of ROS/ASK1/p38 MAPK pathways is responsible for the apoptosis stimulated by OA in cancer cells. Our finding can contribute to a better understanding of molecular mechanisms underlying the antitumor activity of nutritional components.

TAK1-dependent Activation of AP-1 and c-Jun N-terminal Kinase by Receptor Activator of NF-κB

  • Lee, Soo-Woong;Han, Sang-In;Kim, Hong-Hee;Lee, Zang-Hee
    • BMB Reports
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    • 제35권4호
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    • pp.371-376
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    • 2002
  • The receptor activator of nuclear factor kappa B (RANK) is a member of the tumor necrosis factor (TNF) receptor superfamily. It plays a critical role in osteoclast differentiaion, lymph node organogenesis, and mammary gland development. The stimulation of RANK causes the activation of transcription factors NF-${\kappa}B$ and activator protein 1 (AP1), and the mitogen activated protein kinase (MAPK) c-Jun N-terminal kinase (JNK). In the signal transduction of RANK, the recruitment of the adaptor molecules, TNF receptor-associated factors (TRAFs), is and initial cytoplasmic event. Recently, the association of the MAPK kinase kinase, transforming growth factor-$\beta$-activated kinase 1 (TAK1), with TRAF6 was shown to mediate the IL-1 signaling to NF-${\kappa}B$ and JNK. We investigated whether or not TAK1 plays a role in RANK signaling. A dominant-negative form of TAK1 was discovered to abolish the RANK-induced activation of AP1 and JNK. The AP1 activation by TRAF2, TRAF5, and TRAF6 was also greatly suppressed by the dominant-negative TAK1. the inhibitory effect of the TAK1 mutant on RANK-and TRAF-induced NF-${\kappa}B$ activation was also observed, but less efficiently. Our findings indicate that TAK1 is involved in the MAPK cascade and NF-${\kappa}B$ pathway that is activated by RANK.

Control of $Ca^{2+}$- Influx by $Ca^{2+}$/Calmodulin Dependent Protein Kinase II in the Activation of Mouse Eggs

  • Yoon, Sook-Young;Kang, Da-Won;Bae, In-Ha
    • 한국발생생물학회지:발생과생식
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    • 제15권1호
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    • pp.31-39
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    • 2011
  • Change in intracellular $Ca^{2+}$-concentration ($[Ca^{2+}]_i$) is an essential event for egg activation and further development. $Ca^{2+}$ ion is originated from intracellular $Ca^{2+}$-store via inositol 1,4,5-triphosphate receptor and/or $Ca^{2+}$ influx via $Ca^{2+}$ channel. This study was performed to investigate whether changes in $Ca^{2+}$/calmodulin dependent protein kinase II (CaM KII) activity affect $Ca^{2+}$ influx during artificial egg activation with ethanol using $Ca^{2+}$ monitoring system and whole-cell patch clamp technique. Under $Ca^{2+}$ ion-omitted condition, $Ca^{2+}$-oscillation was stopped within 30 min post microinjection of porcine sperm factor, and ethanol-induced $Ca^{2+}$ increase was reduced. To investigate the role of CaM KII known as an integrator of $Ca^{2+}$- oscillation during mammalian egg fertilization, CaM KII activity was tested with a specific inhibitor KN-93. In the eggs treated with KN-93, ethanol failed to induce egg activation. In addition, KN-93 inhibited inward $Ca^{2+}$ current ($I_{Ca}$) in a time-dependent manner in whole-cell configuration. Immunostaining data showed that the voltage-dependent $Ca^{2+}$ channels were distributed along the plasma membrane of mouse egg and 2-cell embryo. From these results, we suggest that $Ca^{2+}$ influx during fertilization might be controlled by CaM KII activity.

PKC Downstream of PI3-Kinase Regulates Peroxynitrite Formation for Nrf2-Mediated GSTA2 Induction

  • Kim, Sang-Geon;Kim, Sun-Ok
    • Archives of Pharmacal Research
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    • 제27권7호
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    • pp.757-762
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    • 2004
  • The protective adaptive response to electrophiles and reactive oxygen species is mediated by the induction of phase II detoxifying genes including glutathione S-transferases (GSTs). NF-E2-related factor-2 (Nrf2) phosphorylation by protein kinase C (PKC) is a critical event for its nuclear translocation in response to oxidative stress. Previously, we have shown that peroxynitrite plays a role in activation of Nrf2 and Nrf2 binding to the antioxidant response element (ARE) via the pathway of phosphatidylinositol 3-kinase (PI3-kinase) and that nitric oxide synthase in hepatocytes is required for GSTA2 induction. In view of the importance of PKC and Pl3-kinase in Nrf2-mediated GST induction, we investigated the role of these kinases in peroxynitrite formation for GSTA2 induction by oxidative stress and determined the relationship between PKC and PI3-kinase. Although PKC activation by phorbol 12-myristate-13-acetate (PMA) did not increase the extents of constitutive and inducible GSTA2 expression, either PKC depletion by PMA or PKC inhibition by staurosporine significantly inhibited GSTA2 induction by tert-butylhydroquinone (t-SHa) a prooxidant chemical. Therefore, the basal PKC activity is req- uisite for GSTA2 induction. 3-Morpholinosydnonimine (SIN-1), which decomposes and yields peroxynitrite, induced GSTA2, which was not inhibited by PKC depletion, but slightly enhanced by PKC activation, suggesting that PKC promotes peroxynitrite formation for Nrf2-mediated GSTA2 induction. Treatment of cells with S-nitroso-N-acetyl-penicillamine (SNAP), an exogenous NO donor, in combination with t-BHQ may produce peroxynitrite. GSTA2 induction by SNAP + t-BHQ was not decreased by PKC depletion, but rather enhanced by PKC activation, showing that the activity of PKC might be required for peroxynitrite formation. LY294002 a P13-kinase inhibitor blocked GSTA2 induction by t-BHQ, which was reversed by PMA-induced PKC activation. These results provide evidence that PKC may playa role in formation of peroxynitrite that activates Nrf2 for GSTA2 induction and that PKC may serve an activator for GSTA2 induction downstream of PI3-kinase.