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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. Jang-Soo Chun is a professor in the school of Life Sciences at Gwangju Institute of Science and Technology (GIST). Dr. Chun received his B.S. and M.S. in biology from Pusan National University and his Ph.D. from University of Massachusetts at Amherst where he studied signal transduction pathways of cell-ECM adhesion under the supervision of Dr. Bruce Jacobson. He did his postdoctoral work in Dr. Merton Bernfield s laboratory at Harvard Medical School/Children s Hospital and investigated the biological functions of the Syndecan, a family of transmembrane sulfate proteoglycans. He joined the Department of Biology at Kyungpook National University as an assistant professor in 1994 and he pioneered signaling mechanisms during chondrogenesis and cartilage development. After he moved to GIST in 2000, he continuously built-up his own research fields that focused on chondrocyte biology, cartilage development and cartilage degeneration. Recently, he made a major breakthrough in the understanding of osteoarthritis (OA) pathogenic mechanisms by identifying the role of hypoxia-inducible factor (HIF)-2a as a catabolic regulator contributing to cartilage destruction. He has been also active in conducting projects for the discovery of novel factors regulating cartilage degeneration and OA pathogenesis. His current interest is on unraveling the molecular pathogenesis of osteoarthritis and developing novel therapeutic approaches for the joint diseases. Dr. Chun is currently the director of the Cell Dynamics Research Center (SRC) supported by Nation Research Foundation of Korea.

Representative papers
- Yang S, Kim J Ryu JH, Oh H, Chun CH, Kim BJ, Min BH, Chun JS. (2010) Hypoxia-inducible factor-2αis a catabolic regulator of osteoarthritic cartilage destruction. Nature Medicine. 16: 687-693.
- Ryu JH, Yang S, Shin Y, Rhee J, Chun CH, Chun JS. (2011) Interleukin 6 plays an essential role in hypoxia-inducible factor-2a-induced experimental osteoarthritic cartilage destruction in mice. Arthritis and Rheumatism. 63: 2732-2743.
- Ryu JH, Shin Y, Huh YH, Yang S, Chun JS. (2012) Hypoxia-inducible factor-2αregulates Fas-mediated chondrocyte apoptosis during osteoarthritic cartilage destruction. Cell Death Differ. 19: 440-450.
- Oh H, Chun CH, Chun JS. (2012) Dickkopf-1 expression in chondrocytes inhibits experimental osteoarthritic cartilage destruction in mice. Arthritis and Rheumatism. 64: 2568-2578.
- Oh H, Ryu JH, Jeon J, Yang S, Chun CH, Park H, Kim HJ, Kim WS, Kim HH, Kwon YG, Chun JS. (2012) Misexpression of Dickkopf-1 in endothelial cells, but not in chondrocytes or hypertrophic chondrocytes, causes defects in endochondral ossification. J Bone Miner Res. 27: 1335-1344.

   

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

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Non-Specific Phytohormonal Induction of AtMYB44 and Suppression of Jasmonate-Responsive Gene Activation in Arabidopsis thaliana. (2010). Mol. Cells 29, 71-76.

The Arabidopsis transcription factor AtMYB44 confers drought/salinity tolerance by enhancing the abscisic acid (ABA) signaling. In this paper, we reported that various phytohormones, including ABA and jasmonates, induced rapid AtMYB44 transcript accumulation, which was not abolished in Arabidopsis mutants insensitive to jasmonates (coi1) or ABA (abi3-1). Seedlings of transgenic Arabidopsis overexpressing the gene exhibited elevated chlorophyll levels and less anthocyanin accumulation, illustrating suppression of jasmonate-mediated responses and enhancement of ABA-mediated responses. Activation of jasmonate-responsive genes was attenuated in overexpression plants, but significantly enhanced in knockout mutants. Both mutant plants did not show defectiveness in MeJA-induced primary root growth inhibition, indicating no alteration in the jasmonate signaling. Thus, AtMYB44 appears not to integrate jasmonate-mediated signaling, but to exert an antagonistic action against the ABA signaling.

   

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