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        Dual Effect of Nerve Growth Factor on Cell Death of PC12 Cells Induced by Serum Deprivation

        KyuChung Hur,Mijung Kwon,Sooryun Seo,Hoyoung Chun,Jun-Mo Chung,In Kwon Chung 한국분자세포생물학회 2002 Molecules and cells Vol.13 No.2

        The effect of nerve growth factor (NGF) on the cell death of PC12 cells that is induced by serum deprivation was examined in the floating and attached cells to the extracellular matrix. NGF suppressed cell death occurred in the floating cells. The onset of cell death in the attached cells was much slower than in the floating cells. Moreover, the cell death in the attached cells was either accelerated in a high-density culture (over ~50% confluent), or inhibited in a low-density culture by NGF. While nucleosomal DNA fragmentation and poly (ADP-ribose) polymerase degradation was observed in both the floating and attached cells, the incidence of nuclear fragmentation and chromatin condensation was much lower in the attached cells than in the floating cells. The delayed onset of cell death in the attached cells was due to the signals that are generated from the extracellular matrix that is formed by PC12 cells, together with cell-to-cell interaction. The acceleration of cell death in the NGF-treated cells was anoikis, caused by the loss of the anchorage of the cell via the action of increased activities of matrix metalloproteinases (MMP2, MMP9). These results suggest that NGF has a different role in the cell death of PC12 cells that is induced by serum deprivation, depending on the cell-matrix, as well as the cell-cell interaction.

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        Thick-film ammonia gas sensor with high sensitivity and excellent selectivity

        Lee, Kyuchung,Ryu, Kwang-Ryul,Hur, Chang-Wu The Korea Institute of Information and Commucation 2004 Journal of information and communication convergen Vol.2 No.1

        A highly sensitive ammonia gas sensor using thick-film technology has been fabricated and examined. The sensing material of the gas sensor is FeOx-$WO_{3}-SnO_{2}$ oxide semiconductor. The sensor exhibits resistance increase upon exposure to low concentration of ammonia gas. The resistance of the sensor is decreased, on the other hand, for exposure to reducing gases such as ethyl alcohol, methane, propane and carbon monoxide. A novel method for detecting ammonia gas quite selectively utilizing a sensor array consisting of an ammonia gas sensor and a compensation element has been proposed and developed. The compensation element is a Pt-doped $WO_{3}-SnO_{2}$gas sensor which shows opposite direction of resistance change in comparison with the ammonia gas sensor upon exposure to ammonia gas. Excellent selectivity has been achieved using the sensor array having two sensing elements.

      • Blockage of K+ efflux Suppresses Staurosporine Induced Apoptosis by Preventing the Formation of the Apaf-1 Apoptosome and the Downstream Pathways

        Seong, Changhyun,Kim, Bo-Eun,Cho, Jinsun,Park, Sung-Hee,Lee, Yun-Hee,Hur, Kyuchung,Park, Il-Seon 이화여자대학교 세포신호전달연구센터 2001 고사리 세포신호전달 심포지움 Vol. No.3

        Upon apoptotic insult cell loses intracelluar K+ and blockage of the efflux by K+ channel blockers or the high concentration of extracelluar K+ suppresses the apoptosis. The suppression of staurosporine induced apoptosis by the blockage was not relieved by inhibitors of protein kinase C, phosphatidylinositol 3-kinase and others. Furthermore, the release of cytochrome C from the mitochondria was neither significantly changed with the blockage of the efflux. Whereas processing of procaspase-9, -3, -8 and other death related proteins completely disappeared with the blockage. Importantly, the blockage of K+ efflux prevented the formation of the apoptosome, a multiprotein complex consisting of cytochrome C, Apaf-1, dATP and caspase-9. Consistently, the formation of the apoptosome induced by dATP and cytochrome C in the cell free system was also significantly inhibited by 150 mM KCl, the normal physiological K+ level. The same concentration of KCl inhibited in different extents processing of procaspase-3 by caspase-8 or 9, nucleosomal DNA fragmentation by purified DFF40/CAD and nuclear fragmentation. Taken together, these results strongly suggest that the protective effect of K+ on the staurosporine-induced apoptosis occurs mainly at a site of the apoptosome formation and this effect seems to be augmented by the inhibition of downstream apoptotic pathways.

      • Caspase Alone Can Induce DNA Fragmentation In Isolated Nuclei

        Lee, Hyun-Jung,Cho, Jinsun,Seong, Chang-Hyun,Kim, Bo-Eun,Lee, Yun-Hee,Hur, Kyuchung,Park, Il-Seon 이화여자대학교 세포신호전달연구센터 2000 고사리 세포신호전달 심포지움 Vol. No.2

        Apoptosis is a programmed cell death characterized by the cellular and nuclear changes including chromosomal DNA fragmentation(DF). For the nuclear DF the activation of pro-caspase to processed caspase, an apoptosis-specific cysteine protease, is required. The protease alone, however, was known to be unable to induce the DF in nucleus(reviewed in Nature, 401:127) and cellular factor(s) such as DFF40/CAD was reported to be necessay. In this study, however, it is shown that the DF can occur by caspase-3 and 7(but not by 6 and 8) without the aid of any cytoplasmic factors. For the maximal DF 50~75 mM NaCl or KCl is necessary. The DF can be inhibited by ICAD protein, the CAD specific inhibitor. Fractionation of nuclear extract by size-exclusion column and the following Western blotting experiments indicates the involvement of DFF40/CAD-related DNase in the process.

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