• B.S., Seoul National University, Seoul, Korea, 1988
• M.S., Seoul National University, Seoul, Korea, 1991
• Ph.D., Seoul National University, Seoul, Korea, 1996
• Research Fellow, Division of Nephrology, Johns Hopkins University, 1996 – 1999
• Research Associate, Division of Nephrology, Johns Hopkins University, 1999 – 2001
• Instructor, Division of Nephrology, Johns Hopkins University, 2001 – 2002
• Assistant Professor , Division of Nephrology, Johns Hopkins University, 2002 – 2006
• Assistant Professor, Department of Neurosurgery, University of Maryland School of Medicine, 2006-present
I was born and raised in Seoul, South Korea and earned my PhD from Seoul National University. My thesis work was to purify and characterize a family of enzymes that cleave peptide or iso-peptide bonds conjugated to ubiquitin. In 1996, I came to Baltimore, Maryland to get Post Doc training at Johns Hopkins Medical School. Since then, my research interests have focused on transcriptional regulation of genes in pathophysiological conditions. Since joining the University Maryland Neurosurgery Department in 2006, my research interest has been investigating a transcriptional program that regulates expression of the SUR1-regulated non-selective cation channel (NCCa-ATP) in CNS pathological conditions.
We have identified a non-selective cation channel (NCCa-ATP) that plays a key role in oncotic cell death following various forms of CNS injury such as stroke and spinal cord injury. Our recent research data indicate the channel is composed of at least two different subunits; one is sulfonylurea receptor 1 (SUR1) as a regulatory subunit and the other is transient receptor potential cation channel, subfamily M, member 4 (TRPM4) as a pore-forming subunit. Importantly, the channel is inactive in normal condition; whereas it becomes activated in the pathological conditions. My research goal is to elucidate activation mechanism of the channel. That includes (1) identification of cis-regulatory elements and trans-acting factors involved in transcriptional stimulation of the SUR1 and TRPM4 genes following ischemic and traumatic CNS injury, and (2) studying post-translational regulatory mechanism including physical interaction between the two subunits and trafficking to plasma membrane. So far, we have identified Sp1, hypoxia inducible factor-1 (HIF-1), NFkB, and sex determining region Y (SRY) as major transcription factors that regulate transcription of the genes in the pathological conditions.
Lab Techniques and EquipmentWe study various animal models as well as in vitro cultured cell lines. We mainly perform biochemical, molecular biological, and cell biological techniques including antibody generation, gene cloning, transfection, gene targeting, qRT-PCR, immunoblot analysis, reporter gene assay, chromatin immunoprecipitation (ChIP), EMSA, immunohistochemistry, etc.
Woo SK, Kwon MS, Geng Z,Ivanov A, Bhatta S, Gerzanich V, Simard JM. (2011) Sequential activation of hypoxia-inducible factor 1 and specificity protein 1 is required for hypoxia-induced transcriptional stimulation of Abcc8. J Cereb Blood Flow Metab. In press
Simard JM, Woo SK,Norenberg MD, Tosun C, Chen Z, Ivanova S, Tsymbalyuk O, Bryan J, Landsman D, Gerzanich V (2010) Brief Suppression of Abcc8 prevents autodestruction of spinal cord after trauma. SciTranl Med. 2(28):28ra29
Gerzanich V, Woo SK, Vennekens R, Tsymbalyuk O, Ivanova S, Ivanov A, Geng Z, Chen Z, Nilius B, Flockerzi V, Freichel M, and Simard JM. (2009) De novo expression of TRPM4 initiates secondary hemorrhage in spinal cord injury. Nat. Med. 15:185-191.
Simard JM, Woo SK, Bhatta S, and Gerzanich V. (2008) Drugs acting on SUR1 to treat CNS ischemia and trauma. CurrOpinPharmacol. 8:42-49.
Simard JM, Tsymbalyuk O, Ivanov A, Ivanova S, Bhatta S, Geng Z, Woo SK, and Gerzanich V. (2007) Endothelial sulfonylurea receptor 1-regulated NC Ca-ATP channels mediate progressive hemorrhagic necrosis following spinal cord injury. J. Clin. Invest. 117:2105-2113.
Sheen MR, Kim SW, Jung JY, Ahn JY, Rhee JG, Kwon HM, and Woo SK. (2006) Mre11-Rad50-Nbs1 (MRN) complex is activated by hypertonicity. Am. J. Physiol. 291:F1014-F1020.
Kim DJ, Park SH, Sheen MR, Jeon US, Kim SW, Koh ES, and Woo SK. (2006) Comparison of experimental lung injury from acute renal failure versus that due to sepsis. Respiration. 73: 815-824.
Woo SK, Lee SD, and Kwon HM. (2002) TonEBP transcriptional activator in the cellular response to increased osmolality.Pflugers Arch. 444: 579-585.
Woo SK, Lee SD, Na KY, Park WK, and Kwon HM. (2002) TonEBP/NFAT5 stimulates transcription of HSP70 in response to hypertoniciy. Mol. Cell. Biol. 22: 5753-5760.
Woo SK, Dahl SC, Handler JS, and Kwon HM. (2000) Bi-directional regulation of tonicity-responsive enhancer binding protein in response to changes in tonicity. Am. J. Physiol., 278; F1006-F1012.
Miyakawa H, Woo SK, Dahl SC, Handler JS, and Kwon HM. (1999) Tonicity-responsive enhancer binding protein, a Rel-like protein that stimulates transcription in response to hypertonicity. Proc. Natl. Acad. Sci. USA, 96, 2538-2542.
Woo SK, Lee JI, Park IK, Yoo YJ, Cho CM, Kang MS, Ha DB, Tanaka K, and Chung CH. (1995) Multiple ubiquitin C-terminal hydrolases from chick skeletal muscle. J. Biol. Chem., 270; 18766-18773.