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1. Çмú»ó (KSMCB Academic Research Awards)

 
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Á¦19ȸ ¼ö»óÀÚ (2020³â) Á¦18ȸ ¼ö»óÀÚ (2019³â) Á¦17ȸ ¼ö»óÀÚ (2018³â) Á¦16ȸ ¼ö»óÀÚ (2017³â)
Á¦15ȸ ¼ö»óÀÚ (2016³â) Á¦14ȸ ¼ö»óÀÚ (2015³â) Á¦13ȸ ¼ö»óÀÚ (2014³â) Á¦12ȸ ¼ö»óÀÚ (2013³â)
Á¦11ȸ ¼ö»óÀÚ (2012³â) Á¦10ȸ ¼ö»óÀÚ (2011³â) Á¦9ȸ ¼ö»óÀÚ (2010³â) Á¦8ȸ ¼ö»óÀÚ (2009³â)
Á¦7ȸ ¼ö»óÀÚ (2008³â) Á¦6ȸ ¼ö»óÀÚ (2007³â) Á¦5ȸ ¼ö»óÀÚ (2006³â) Á¦4ȸ ¼ö»óÀÚ (2005³â)
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(1994³â-2000³â)
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Dr. Young-Yun Kong is a Professor in the Department of Biological Sciences at Seoul National University. He received his bachelor's degree and master's degree at KyungHee University, and Ph.D. degree in the Medical Institute of Bioregulation at the Kyushu University in 1996. During his graduate studies in the laboratory of Dr. Kikuo Nomoto in Japan, he investigated the differential role of CD45 in the T and B lymphocyte function. During his postdoctoral training under the guidance of Dr. Josef Penninger in the Amgen/Ontario Cancer Institute at the University of Toronto, he generated OPGL/RANKL knockout mice and demonstrated that OPGL is a key factor for osteoclastogenesis and lymph node formation. He joined Pohang University of Science and Technology as an assistant Professor in 2000 and generated various mouse genetic models including E3 ubiquitin ligases, Mib1, Mib2, Neur1 and Neur2 that regulate Notch ligands. In mammals, he proved that Mib1 plays an obligatory role in Notch signaling in the various developmental contexts. Using these genetic models, he found that Mind bomb 1-expressing intermediate progenitors generate Notch signaling to maintain radial glial cells during forebrain development. He extended his work to Notch signaling in the generation of hematopoietic stem cells at the aorta-mesonephros-gonad, Notch signaling in the microenvironment that regulates hematopoiesis in the bone marrow, Notch signaling in the lymphopoietic niches that regulate T and marginal zone B cell development, and Notch signaling in the Eph-Ephrin boundary formation of the intestine. He moved to Seoul National University in 2008. Since then, he further extended his work to Notch signaling in renal collecting duct development and found that defect of Notch signaling results in nephrogenic diabetes insipidus. Moreover, his group demonstrated that Notch signaling counteracts WNT/¥â-catenin signaling through chromatin modification in colorectal cancer. Recently, he has been interested in skeletal muscle stem cells. He found that sex hormones establish a reserve pool of adult muscle stem cells by regulating Notch signaling at puberty. His current studies are attempting to solve the role of sex hormones in the maintenance and re-establishment of muscle stem cells after injury and then finally aging and rejuvenation of muscle stem cells.

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1. Sex hormones establish a reserve pool of adult muscle stem cells. Nat Cell Biol. 18:930-40 (2016)
2. Notch1 counteracts WNT/¥â-catenin signaling through chromatin modification in colorectal cancer. J Clin Invest. 122:3248-59 (2012)
3. CRIF1 is essential for the synthesis and insertion of oxidative phosphorylation polypeptides in the mammalian mitochondrial membrane. Cell Metab. 16:274-83 (2012)
4. Notch Signaling Promotes the Generation of EphrinB1-Positive Intestinal Epithelial Cells. Gastroenterology. 137:145?155 (2009)
5. Mind bomb 1-expressing intermediate progenitors generate Notch signaling to maintain radial glial cells. Neuron, 58:519-531 (2008)

   

Çѱ¹ºÐÀÚ·¼¼Æ÷»ý¹°ÇÐȸ Çмú»ó Molecules and Cells (M&C) ¿ì¼ö³í¹®»ó ¼ö»óÀÚ

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A Long Non-Coding RNA snaR Contributes to 5-Fluorouracil Resistance in Human Colon Cancer Cells (Mol. Cells 2014; 37(7): 540-546)

Eun Kyung Lee, Ph.D. Department of Biochemistry, College of Medicine, The Catholic University of Korea Several types of genetic and epigenetic regulation have been implicated in the development of drug resistance, one significant challenge for cancer therapy. Although changes in the expression of non-coding RNA are also responsible for drug resistance, the specific identities and roles of them remain to be elucidated. Long non-coding RNAs (lncRNAs) are a type of ncRNA (> 200 nt) that influence the regulation of gene expression in various ways. In this study, we aimed to identify differentially expressed lncRNAs in 5-fluorouracil-resistant colon cancer cells. Using two pairs of 5-FU-resistant cells derived from the human colon cancer cell lines SNU-C4 and SNU-C5, we analyzed the expression of 90 lncRNAs by qPCR-based profiling and found that 19 and 23 lncRNAs were differentially expressed in SNU-C4R and SNU-C5R cells, respectively. We confirmed that snaR and BACE1AS were downregulated in resistant cells. To further investigate the effects of snaR on cell growth, cell viability and cell cycle were analyzed after transfection of siRNAs targeting snaR. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. Our results provide an important insight into the involvement of lncRNAs in 5-FU resistance in colon cancer cells.

   

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