• Youngsoo Kim
  • Sang-Bae Han
Youngsoo Kim
043-261-2823
youngsoo@chungbuk.ac.kr

Education & Career

 1977-1981: BS, College of Pharmacy, Chungbuk National University, Korea
 1981-1983: MS, College of Pharmacy, Seoul National University, Korea
 1984-1988: Ph.D, Dept. of Biochemical & Biophysical Sciences, University of Houston, USA
 1988-1989: Post-Doc, Division of Applied Toxicology, MIT, USA
 1989-1998: Assistant & Associate Professor, College of Pharmacy, Chungbuk National University
 1998-present: Full professor, College of Pharmacy, Chungbuk National University
 2004-2005: Dean, College of Pharmacy, Chungbuk National University
 2006-2013: BK21 Director, Frontier Pharmaceutical Technology for Biotopia
 2007-2008: Chairman, Division of Pharmaceutical Biochemistry, The Pharmaceutical Society of Korea
 2008-2010: Director of Research Institute, Development of Pharmaceutical Resources, Chungbuk National University
 2013-present: BK21+ Director, Frontier Pharmacy Leaders
 2015-present: Vice President, The Pharmaceutical Society of Korea

 

International Collaboration & Short Visiting Abroad

 2001. 7: Univ. of Tokyo, Japan (Prof. Kyioshi Takatsu & IL-5)
 1998. 7: Tohoku Univ., Japan (Prof. Kazuo Ohuchi & Inflammatory signaling)
 1997. 1: Chiba Univ., Japan (Prof. Shingo Yano & Hypersensitivity models)
 1996. 8: Toyama Medical & Pharmaceutical Univ., Japan (Prof. Hideo Nakagawa & Chemokine)
 1996. 1: Osaka Univ. School of Medicine, Japan (Prof. Toshio Hirano & IL-6)
 1994. 7: Michigan State Univ., USA (Prof. Bill Smith & Prostanoids)

 

Research Areas

 1) Drug Discovery Targeting Toll-like Receptor and Signal Transduction

 2) Drug Discovery against Skin Hyperpigmentation


 

Selected Publications

1) Yun C-Y, Ko SM, Choi YP, Kim BJ, Lee JR, Kim JM, Kim JY, Song JY, Kim SH, Hwang BY, Hong JT, Han S-B, Kim Y. Alpha-viniferin improves facial hyperpigmentation via accelerating feedback termination of cAMP/PKA-signaled phosphorylation circuit in facultative melanogenesis. Theranosctics 9: 2031-2043 (2018)

2) Park SH, Kwak JA, Jung SH, Ahn B, Cho WJ, Yun C-Y, Na CS, Hwang BY, Hong JT, Han S-B, Kim Y. Piperidylmethyloxychalcone improves immune-mediated acute liver failure via inhibiting TAK1 activity. Exp. Mol. Med. 49: e392 (2017)

3) Boggu PR, Venkateswararao E, Manickam M, Kim Y, Jung SH. Discovery of novel 3-(hydroxyalkoxy)-2-alkylchromone-4-one analogs as interleukin-5 inhibitors. Eur. J. Med. Chem. 139: 290-304 (2017)

4) Choi JH, Park SH, Jung JK, Cho WJ, Ahn B, Yun C-Y, Yeo JW, Lee H, Hong JT, Han S-B, Kim Y. Caffeic acid cyclohexylamide rescues lethal inflammation in septic mice through inhibition of IkB kinase in innate immune process. Sci. Rep. 7: 41180 (2017)

5) Boggu PR, Venkateswararao E, Manickam M, Kwak DJ, Kim Y, Jung SH. Exploration of 2-benzylbenzimidazole scaffold as novel inhibitor of NF-kB. Bioorg. Med. Chem. 24: 1872-1878 (2016)

6) Shin H, Hong SD, Roh E, Jung SH, Cho WJ, Park SH, Yoon DY, Ko SM, Hwang BY, Hong JT, Heo T-Y, Han S-B, Kim Y. cAMP-dependent activation of protein kinase A as a therapeutic target of skin hyperpigmentation by diphenylmethylene hydrazinecarbothioamide. Br. J. Pharmacol. 172: 3434-3445 (2015)

7) Park SH, Baek S-I, Yun J, Lee S, Yoon DY, Jung JK, Jung SH, Hwang BY, Hong JT, Han S-B, Kim Y. IRAK4 as a molecular target in the amelioration of innate immunity-related endotoxic shock and acute liver injury by chlorogenic acid. J. Immunol. 194: 1122-1130 (2015)

8) Roh E, Jeong I-Y, Shin H, Song S, Hong JT, Lee S, Han S-B, Kim Y. Downregulation of melanocyte-specific facultative melanogenesis by 4-hydroxy-3-methoxycinnamaldehyde acting as a cAMP antagonist. J. Invest. Dermatol. 134: 551-553 (2014)

9) Park SH, Roh E, Kim HS, Baek S-I, Choi NS, Kim N, Hwang BY, Han S-B, Kim Y. Inhibition of IRAK-4 activity for rescuring endotoxin LPS-induced septic mortality in mice by lonicerae flos extract. Biochem. Biophys. Res. Commun. 442: 183-184 (2013)

10) Roh E, Yun C-Y, Yun JY, Park D, Kim ND, Hwang BY, Jung SH, Park SK, Kim Y-B, Han S-B, Kim Y. cAMP-binding site of PKA as a molecular target of bisabolangelone against melanocyte-specific hyperpigmented disorder. J. Invest. Dermatol. 133: 1072-1079 (2013)

 

Sang-Bae Han
043-261-2815
shan@chungbuk.ac.kr

Education:  

1988-1992: BS, College of Pharmacy, Chungbuk National University
1992-1994: MS, College of Pharmacy, Chungbuk National University
1998-2001: Ph.D, Department of Biological Sciences, KAIST


Career

1992-2007: Senior Research Scientist, KRIBB, Korea
2003-2004: Post Doc, NIAID, NIH, USA
2007-present: Professor, College of Pharmacy, Chungbuk National University
2011-2013: Chief, Department of Pharmacy, College of Pharmacy, Chungbuk National University
2015-2017: Vice dean, College of Pharmacy, Chungbuk National University


Selected Publications

1) Rgs1 and Gnai2 regulate the entrance of B lymphocytes into lymph nodes and B cell motility within lymph node follicles. Han SB, Moratz C, Huang NN, Kelsall B, Cho H, Shi CS, Schwartz O, Kehrl JH. Immunity. 2005 Mar;22(3):343-54.
2) Tussilagone inhibits dendritic cell functions via induction of heme oxygenase-1. Park Y, Ryu HS, Lee HK, Kim JS, Yun J, Kang JS, Hwang BY, Hong JT, Kim Y, Han SB. Int Immunopharmacol. 2014 Oct;22(2):400-8.
3) Platycodon grandiflorum polysaccharide induces dendritic cell maturation via TLR4 signaling. Park MJ, Ryu HS, Kim JS, Lee HK, Kang JS, Yun J, Kim SY, Lee MK, Hong JT, Kim Y, Han SB. Food Chem Toxicol. 2014 Oct;72:212-20.
4) Saucerneol D inhibits dendritic cell activation by inducing heme oxygenase-1, but not by directly inhibiting toll-like receptor 4 signaling. Ryu HS, Lee HK, Kim JS, Kim YG, Pyo M, Yun J, Hwang BY, Hong JT, Kim Y, Han SB. J Ethnopharmacol. 2015 May 26;166:92-101.


Research Areas

1) Immune cell therapy of cancer

Natural killer (NK) cells are large granular lymphocytes capable of clearing both virus-infected and transformed cells. NK cell cytotoxicity is controlled by the integration of activating and inhibitory receptor signaling at the NK cell immune synapse (IS) formed between NK and target cells. NK cells can also respond by producing cytokines, e.g., interferon-γ (IFN-γ) or tumor necrosis factor-α (TNF-α), and are known to be activated by cytokines like interleukin (IL)-2, IL-12, and IL-15. Activating receptors, such as DNAM-1, NKp44, and KLRB1, are upregulated, while inhibitory receptors, like KIR2DL2 and KIR3DL3, are downregulated after exposure to IL-2. In addition, increased cell-cell adhesion has been directly coupled to cytotoxicity. NK cells are able to lyse target cells but require the right combination of activating signals, and, therefore, seem more tightly regulated than IL-2-activated NK cells. In our lab, we are focusing on the identification of cytotoxic dynamics of NK cells. Using time-lapse imaging, we examine "cytotoxic dynamics", such as killing behavior, contact dynamics, motility and directionality of NK cells as well as dying process of cancer cells.


2) Mesenchymal stem cell therapy of autoimmune diseases

Mesenchymal stem cells (MSCs) are present in diverse tissues and organs, including bone marrow, umbilical cord, adipose tissue, and placenta. MSCs can expand easily in vitro and have regenerative stem cell properties and potent immunoregulatory activity. They inhibit the functions of dendritic cells, B cells, and T cells, but enhance those of regulatory T cells by producing immunoregulatory molecules such as transforming growth factor-β, hepatic growth factors, prostaglandin E2, interleukin-10, indolamine 2,3-dioxygenase, nitric oxide, heme oxygenase-1, and human leukocyte antigen-G. These properties make MSCs promising therapeutic candidates for the treatment of autoimmune diseases. However, the detailed mechanisms by which MSCs exert their immunomodulatory functions are still incompletely understood. In our lab, we focus on identifying the immunoregulatory mechanisms of MSCs. Our hypothesis is that MSCs might regulate the functions of immune cells (T cells, B cells, dendritic cells, and so on) via producing soluble mediators and direct cell-cell contact. To prove it, two strategies are established. First, we are trying to identify cell-type-specific soluble mediator. Second, using time-lapse imaging, we are studying the cell type-specific contact dynamics, such as contact duration, contact frequency, motility speeds, directionality, and their relevance with chemokine axis.


3) ) Immuno- & Onco-pharmacology

Our lab has assay systems to evaluate the efficacy of immunomodulators (stimulants and suppressants). In enzymatic assay, we general identify the direct molecular target of compounds by using kinase assay. In cellular assay, we generally test the effect of compounds on viability, proliferation and Ab production of B cells, proliferation and cytokine production of T cells, maturation of dendritic cells (6 assay parameters), and cytokine production of macrophages. In addition, we examine the effect of compounds on signaling pathways downstream from TCR, BCR, TLRs, and cytokine receptors. In animal assay, we have syngeneic tumor model (tumor growth and metastasis) to develop immunostimulants and inflammation models (lupus and rheumatoid arthritis) to develop anti-inflammatory drugs. We also have assay systems to evaluate the efficacy and mechanisms of anti-cancer drug candidates. In enzymatic assay, we general identify the direct molecular target of compounds by using kinase assay. In cellular assays, we examine the cytotoxic potential of compounds on more than 60 human cancer cell lines by using SRB, MTT, and SRB assay (for tumor growth inhibitor). We also examine the invasion and migration of endothelial cells (for angiogenesis blocker) and cancer cells (for metastasis inhibitor). We used qRT-PCR to examine the effects of compounds on gene expression and WB on protein expression/phosphorylation. In animal assay, we have syngeneic murine tumor model, xenograft human tumor model (nude mice), and lung metastasis models.