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1. Çмú»ó (KSMCB Academic Research Awards)

 
Á¦22ȸ ¼ö»óÀÚ (2023³â) Á¦21ȸ ¼ö»óÀÚ (2022³â) Á¦20ȸ ¼ö»óÀÚ (2021³â)
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)
Á¦3ȸ ¼ö»óÀÚ (2004³â) Á¦2ȸ ¼ö»óÀÚ (2003³â) Á¦1ȸ ¼ö»óÀÚ (2002³â) ¸ñ¾Ï»ý¸í°úÇлó
(1994³â-2000³â)
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Dr. Hueng-Sik Choi is a Professor in the School of Biological Sciences and Technology at Chonnam National University in Gwangju. He received his bachelor's degree in Biology from Kyung-Hee University and earned his Ph.D. in Dept. of Cell and Developmental Biology at Rutgers University & UMNJ Medical School. During his graduate training, he studied heat shock gene expression in association with cellular aging. He received post-doctoral training in the laboratory of Dr. David D. Moore at Massachusetts General Hospital, Harvard Medical School, and discovered the orphan nuclear receptor, small heterodimer partner (SHP). He joined Chonnam National University as a Full-Time Instructor in 1996 and became Assistant Professor in 1998. He was promoted to Associate Professor in 2002 and Professor in 2008.

His research has been focused mainly on the function of SHP in an attempt to elucidate the molecular mechanisms underlying the regulation of gene expression involved in liver metabolism. He first provided the information on structure and location of the human SHP genome. Moreover, he also demonstrated that AMPK signaling regulates SHP gene expression, which in turn inhibits hepatic gluconeogenesis. Recently, he has been intensively involved in studying the basic mechanism of estrogen-related receptor gamma (ERR) action on metabolic homeostasis to explain molecular etiology of diabetes, obesity, alcoholic liver injury and infectious diseases. As a result, his group discovered that ERR plays an important role in hepatic gluconeogenesis and lipid metabolism involved in insulin resistance and type 2 diabetes. Lately, he showed that ERR controls CYP2E1 expression and alcoholic liver injury. In addition, he expended his work to ERR in iron metabolism and found that ERR controls bacterial infection by modulating host iron metabolism. Finally, he has gone on to prove that inhibition of ERR by its inverse agonist could control bacterial infection, and ameliorate alcoholic liver injury and type 2 diabetes. His current studies are focusing on the role of nuclear receptors in an attempt to understand the biological mechanisms that regulate endocrine and metabolic dysfunction and the interorgan communications that coordinate cellular and systemic integration of homeostasis.

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1. ERR: a Junior Orphan with a Senior Role in Metabolism (2017).Trends Endocrinol Metab. 28:261-272.
2. O-GlcNAcylation of orphan nuclear receptor estrogen-related receptor promotes hepatic gluconeogenesis (2016). Diabetes. 65:2835-2848.
3. Inverse agonist of estrogen-related receptor gamma controls Salmonella typhimurium infection by modulating host iron homeostasis (2014). Nat Med. 20:419-424.
4. Estrogen-related receptor gamma controls hepatic CB1 receptor-mediated CYP2E1 expression and oxidative liver injury by alcohol (2013). Gut. 62:1044-1054.
5. The orphan nuclear receptor SHP acts as a negative regulator in inflammatory signaling triggered by Toll-like receptors (2011). Nat Immunol. 12:742-751.

   

Çѱ¹ºÐÀÚ·¼¼Æ÷»ý¹°ÇÐȸ Çмú»ó Molecules and Cells (M&C) ¿ì¼ö³í¹®»ó ¼ö»óÀÚ
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PLGA-Loaded Gold-Nanoparticles Precipitated with Quercetin Downregulate HDAC-Akt Activities Controlling Proliferation and Activate p53-ROS Crosstalk to Induce Apoptosis in Hepatocarcinoma Cells (2015). Mol. Cells 38, 518-527 Controlled release of medications remains the most convenient way to deliver drugs. In this study, we precipitated gold nanoparticles with quercetin. We loaded gold-quercetin into poly(DL-lactide-co-glycolide) nanoparticles (NQ) and tested the biological activity of NQ on HepG2 hepatocarcinoma cells to acquire the sustained release property. We determined by circular dichroism spectroscopy that NQ effectively caused conformational changes in DNA and modulated different proteins related to epigenetic modifications and c ell cycle control. The mitochondrial membrane potential (MMP), reactive oxygen species (ROS), cell cycle, apoptosis, DNA damage, and caspase 3 activity were analyzed by flow cytometry, and the expression profiles of different anti- and pro-apoptotic as well as epigenetic signals were studied by immunoblotting. A cytotoxicity assay indicated that NQ preferentially killed cancer cells, compared to normal cells. NQ interacted with HepG2 cell DNA and reduced histone deacetylases to control cell proliferation and arrest the cell cycle at the sub-G stage. Activities of cell cycle-related proteins, such as p21WAF, cdk1, and pAkt, were modulated. NQ induced apoptosis in HepG2 cells by activating p53-ROS crosstalk and induces epigenetic modifications leading to inhibited proliferation and cell cycle arrest.

   

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