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Molecular Cloning and Expression of Inositol 1,4,5 - Triphosphate 3 Kinase
Moon, Kyung Ho,Kim, Jae Won,Rhee, Sue Goo,KIM, HA KUN,Lee, Sang Yeol,Choi, Kwan Yong,Chung, Hong Keun,Sin, Sang Soo 한국유전학회 1990 Genes & Genomics Vol.12 No.4
Department of Life Science, Pohang Institute of Science and Technology, Pohang, Korea, *^Department of Biochemistry, Kyongsang National University, Chinju, Korea, (**)^Department of Biochemistry, Kyongsung University, Pusan, Korea, (++)^Department of Biochemistry, College of Medicine, Seoul National University, Seoul, Korea, +^Laboratory of Biochemistry, NHLBI, N.I.H., Bethesda, MD 20892, U.S.A.
Moon, Sang-Kwan,Jin, Hyung-Seok,Ko, Chang-Nam,Kim, Young-Suk,Bae, Hyung-Sup,Lee, Kyung-Sup,Cho, Ki-Ho KYUNG HEE UNIVERSITY MEDICAL CENTER 2006 고황의학상 수상논문집 Vol.21-22 No.-
The effects of Gami-Jeonggi-San (GJS) on proliferation of human endothelial cell (HUV-EC-C) were investigated using a flow cytometry and a quantitative RT-PCR analysis of gene expression. An accumulation of cells at G_(1) phase of the cell cycle was found at 72h after treatment (10 μl/ml) while no detectable reduction of PCNA expression was recognized. To elucidate that the cell cycle inhibitory effect of GJS stems from its capability of transcriptional regulation of the cell cycle-controlling genes, we investigated mRNA expression of p53, Waf1, PCNA, Cyclin D1, Cdc2, Histone H3, c-Myc, and c-Fos. Significantly elevated mRNA levels of the p53 tumor suppressor gene and its down-stream mediator gene, Waf1, whose increased expressions were known to trigger G_(1) cell cycle arrest, were observed. In contrast, a marked reduction of two early G_(1)-specific, cell cycle stimulating genes, c-Myc and c-Fos, were found at 24h after treatment, while there were no detectable changes in expressions of G_(1)-S or G_(2)-M transition-related genes, indicating the G_(1) specificity of GJS effect on the cell cycle. These results suggest that the pharmacological effects of GJS might be derived in part from inhibition of cellular proliferation of human endothelial cells, and that GJS inhibition of the cell cycle might stem from its regulatory capability on the transcription of the cell cycle-controlling genes, including p53 and Waf1 tumor suppressor genes.
Moon, Sang-Kwan,Jin, Hyung-Seok,Ko, Chang-Nam,Kim, Young-Suk,Bae, Hyung-sup,Lee, Kyung-Sup,Cho, Ki-Ho EAST-WEST MEDICAL RESEARCH INSTITUTE KYUNG HEE UNI 2005 東西醫學硏究所 論文集 Vol.2005 No.-
The effects of Gami-Jeonggi-San (GJS) on proliferation of human endothelial cell (HUV-EC-C) were investigated using a flow cytometry and a quantitative RT-PCR analysis of gene expression. An accumulation of cells at G_(1) phase of the cell cycle was found at 72 after treatment (10㎕/㎖) while no detectable reduction of PCNA expression was recognized. To elucidate that the cell cycle inhibitory effect of GJS stems from its capability of transcriptional regulation of the cell cycle-controlling genes, we investigated mRNA expression of p53, Waf1, PCNA, Cyclin D1, Cdc2, Histone H3, c-Myc, and c-Fos. Significantly elevated mRNA levels of the p53 tumor suppressor gene and its down-stream mediator gene, Waf1, whose increased expressions were known to trigger G_(1) cell cycle arrest, were observed. In contrast, a marked reduction of two early G_(1)-specific, cell cycle stimulating genes, c-Myc and c-Fos were found at 24h after treatment, while there were no detectable changes in expressions of G_(1)-S or G_(2)-M transition-related genes, indicating the G_(1) specificity of GJS effect on the cell cycle. These results suggest that the pharmacological effects of GJS might be derived in part from inhibition of cellular proliferation of human endothelial cells, and that GJS inhibition of the cell cycle might stem from its regulatory capability on the transcription of the cell cycle-controlling genes, including p53 and Waf1 tumor suppressor genes.
Sung, Young Kwan,Hwang, Sun Young,Farooq, Mohammad,Kim, Jung-Chul,Kim, Moon Kyu 경북대학교 병원 2003 경북대학교병원의학연구소논문집 Vol.7 No.1
Glypican-3(GPC3) encodes a cell-surface heparan-sulfate proteoglycan and its expression is frequently silenced in ovarian cancer, mesotheliomas, and breast cancer cell lines and ectopic expression of GPC3 inhibited the growth of these cells, suggesting that GPC3 plays a negative role in cell proliferation. In contrast, up-regulation of GPC3 is often observed in hepatoma, neuroblastoma, and Wilms' tumor. Whether GPC3 plays the same growth inhibitory role in these tumors remains to be studied. Here we report that antisense-mediated knockdown of GPC3 in the HepG2 hepatoma cells significantly promotes the growth of hepatoma cells. In addition, we show that this growth promotion is independent of insulin-like growth factor 2(IGF2) signaling. Our data suggest that GPC3 plays a growth-suppressing role in hepatoma and provide cell biological evidence in consistent with the hypothesis that GPC3 acts as a growth suppressor by downregulating IGF2.