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GULLIVER'S TROUBLES IN HIS METAMORPHOSIS
GHILL, BYOUNG-SUP 全北大學校 1982 論文集 Vol.24 No.-
本考는 Gulliver 여행기에 나오는 主人公 話者인 Gulliver 가 作家 Jonathan Swift의 諷刺的 意圖를 充足 시키기 위해 創造된 虛構的 人物이라는 前提를 바탕으로 論旨를 전개하였다. 本考의 硏究目的은 作家와 話者, 讀者 간에 일어나는 同一視 혹은 分離등을 流動性있는 審美的 거리 槪念으로 說明하고, 이 論議에 存在하여 Gulliver 여행기중 Gulliver의 變貌하는 役割을 살피고, 特히 4부의 諷刺的 意味와 方法을 밝히는 데 있다. 1장에서는 本考 硏究의 爭點 및 目的, 方法을 提示하였다. 2장에서는 Swift의 Gulliver 여행기에서 보여지는 諷刺가 直接的이라기 보다는 間接的임을 들어 作家와 作中話者를 全的으로 同一視하는 見解를 批判하였다. 아울러 Gulliver 여행기처럼 寓意性이 짙은 諷刺的 作品에서는 小說이나 戱曲의 作中人物들처럼 作家와 전혀 別個의 '立體的인 個人'을 作中話者로 내세울 수는 없으며 그는 作家의 意見을 直接, 間接으로 反影한다는 것을 밝혔다. 3장에서는 小人國, 大人國, 나는 Laputa 섬 및 기타 地域에 對한 Gulliver 의 3차여행과정 중 Swift 의 諷刺的 目的에 따라 變化하는 Gulliver의 役割을 주로 觀點 分析 方式에 依存하여 살펴 보았다. 4장에서는 Gulliver 여행기 중 가장 批評界의 爭點이 되어있는 馬人國紀行의 意味, 方法에 對해 從來 있어온 解釋의 誤謬를 指摘하였다. 또한 앞의 論議들에 힘입어 作家와 作中話者, 讀者에게 모두 적용되는 풍자의 對象인 人間共通의 惡德인 自慢心에 關해 論議하였다.
Phospholipase C-β3 Mediates the Thrombin-induced Ca2+ Response in Glial Cells
Pann-Ghill Suh,Jong-Ik Hwang,Kum-Joo Shin,Yong-Seok Oh,Jung-Woong Choi,이지원,Daesoo Kim,Kwon-Soo Ha,신희섭,Sung Ho Ryu 한국분자세포생물학회 2005 Molecules and cells Vol.19 No.3
Phospholipase C-β (PLC-β) hydrolyses phosphatidylinositol 4,5-bisphosphate and generates inositol 1,4,5-trisphosphate in response to activation of various G protein-coupled receptors (GPCRs). Using glial cells from knock-out mice lacking either PLC-β1 [PLC-β1 (-/-)] or PLC-β3 [PLC-β3 (-/-)], we examined which isotype of PLC-β participated in the cellular signaling events triggered by thrombin. Generation of inositol phosphates (IPs) was enhanced by thrombin in PLC- β1 (-/-) cells, but was negligible in PLC-β3 (-/-) cells. Expression of PLC-β3 in PLC-β3 (-/-) cells resulted in an increase in pertussis toxin (PTx)-sensitive IPs in response to thrombin as well as to PAR1-specific peptide, while expression of PLC-β1 in PLC-β1 (-/-) cells did not have any effect on IP generation. The thrombin-induced [Ca2+]i increase was delayed and attenuated in PLC-β3 (-/-) cells, but normal in PLC-β1 (-/-) cells. Pertussis toxin evoked a delayed [Ca2+]i increase in PLC-β3 (-/-) cells as well as in PLC-β1 (-/-) cells. These results suggest that activation of PLC-β3 by pertussis toxin-sensitive G proteins is responsible for the transient [Ca2+]i increase in response to thrombin, whereas the delayed [Ca2+]i increase may be due to activation of some other PLC, such as PLC-β4, acting via PTx-insensitive G proteins.
Suh,Pann-Ghill,Ryu,Sung Ho,Kim,Yong,Kim,Su-Jeong,Si,Fu Chun,Kim,Myung Jong The Korea Science and Technology Center 2000 BMB Reports Vol.33 No.2
Phosphoinositide-specific phospholipase C-γ1(PLC-γ1) is a pivotal mediator in the signal transduction cascades induced by many growth factors. Using a yeast two-hybrid system, heat-shock protein 90(Hsp90) was identified as a PLC-γ1-binding protein. A co-immunoprecipitation experiment, using anti-PLC-γ1 antibody, demonstrated an in vivo interaction between Hsp90 and PLC-γ1 in the NIH-3T3 cells. The interaction in NIH-3T3 was unaffected by the PDGF treatment, inducing phosphorylation and activation of PLC-γ1. Direct interaction between Hsp90 and PLC-γ1 was confirmed by in vitro binding experiments using purified Hsp90 and PLC-γ1. Furthermore, Hsp90 increased the PIP₂-hydrolyzing activity of PLC-γ1 up to 2-fold at 0.1μM in vitro. Taken together, we show for the first time, the interaction of PLC-γ1 with Hsp90, both in vivo and in vitro. We suggest that Hsp90 may play a role in PLC-γ1-mediated signal transduction.