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Han Seok Ko, Ph.D.
Associate Professor of Neurology
Research Interests: Molecular and Cellular Signals Controlling Neurodegeneration; Parkinson's disease
Dr. Han Seok Ko obtained his Ph.D. in Pharmacology in 2003 at Hokkaido University in Japan. He then began his postdoctoral fellowship in the Institute for Cell Engineering, Department of Neurology at the Johns Hopkins School of Medicine in Baltimore (USA). There, Han Seok Ko studied Parkinson’s disease (PD).
In particular, his research focused on understanding the molecular mechanisms by which mutations in genes such as parkin, PINK1, DJ-1, LRRK2, and alpha-synuclein, cause PD. He became an Assistant Professor in the Department of Neurology at the Johns Hopkins University School of Medicine in 2010.
Currently, Han Seok Ko is an independent faculty member of the Neuroregeneration Program within the Institute for Cell Engineering, and is a principal investigator of the Morris K. Udall Parkinson’s Disease Research Center of Excellence.
His research goal is to understand the molecular mechanisms driving the loss of brain cells in Parkinson’s disease patients. A clear understanding of both the normal biology and the pathobiology of gene products associated with PD is necessary to gain important insight into the molecular mechanisms and pathways underlying neurodegeneration in PD. Such research has the potential to elucidate novel therapeutic strategies for treatment or prevention of parkinsonian type diseases. To achieve these goals, we utilize a combination of genetically modified animal models to study disease pathogenesis in vivo and neurobiological approaches in vitro. Ongoing projects in the lab include:
- Mechanisms of neurodegeneration in human alpha-synuclein transgenic mice.
- The interaction between Glucocerebrosidase (GBA) and Parkinson’s disease.
- Identification and characterization of important pathophysiologic substrates of parkin that link parkin function to familial and sporadic PD.
PATENT: #C10582-PARIS, a parkin substrate, transcriptionally represses PGC-lot leading to neurodegeneration in Parkinson''s disease. J.H. Shin, H.S. Ko, V.L. Dawson, T.M. Dawson. September 28, 2011
- Associate Professor of Neurology
Departments / Divisions
- Neurology - Institute for Cell Engineering
Centers & Institutes
- B.S., Konkuk University (Korea) (1991)
- Ph.D., Hokkaido University (Japan) (2003)
The Johns Hopkins School of Medicine, Baltimore, MD, 2008, Neurobiology
Research & Publications
Molecular mechanisms driving the loss of brain cells in Parkinson’s disease patients.
The Ko lab studies the molecular mechanisms underlying Parkinson’s disease —a progressive, neurodegenerative movement disorder. By studying the genes responsible for inherited cases of the disease, the researchers aim to understand the cause underlying both sporadic and familial Parkinson’s disease. One such gene codes for the alpha-synuclein protein, which forms insoluble, toxic fibrils in the cells of Parkinson’s disease patients and contributes to neurodegeneration. The Ko lab is characterizing the in vivo relationships between mitochondrial dysfunction, oxidative stress and alpha-synuclein pathology. By studying genetic and biochemical abnormalities of glucocerebrosidase (GBA), an enzyme involved in glycolipid metabolism, the team strives to elucidate how GBA contributes to the pathogenesis in Parkinson’s disease and other disorders characterized by abnormal alpha-synuclein pathologies. The research group is creating animal models that accurately mimic the slow nerve cell death in Parkinson’s disease. By establishing induced pluripotent stem (iPS) cells from Parkinson’s disease patients, the Ko lab plans to study the disease in human dopamine neurons.
Ko’s research has the potential to reveal drug targets, improve early diagnosis and develop new animal models for the study of Parkinson’s disease.
Selected PublicationsView all on Pubmed
- Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss. Lee Y, Karuppagounder SS, Shin JH, Lee YI, Ko HS, Swing D, Jiang H, Kang SU, Lee BD, Kang HC, Kim D, Tessarollo L, Dawson VL, Dawson TM. Nat Neurosci. 2013 Oct;16(10):1392-400. doi: 10.1038/nn.3500. Epub 2013 Aug 25. PMID: 23974709
- Sulfhydration mediates neuroprotective actions of parkin. Vandiver MS, Paul BD, Xu R, Karuppagounder S, Rao F, Snowman AM, Ko HS, Lee YI, Dawson VL, Dawson TM, Sen N, Snyder SH. Nat Commun. 2013;4:1626. doi: 10.1038/ncomms2623. PMID: 23535647
- Iduna is a poly(ADP-ribose) (PAR)-dependent E3 ubiquitin ligase that regulates DNA damage. Kang HC, Lee YI, Shin JH, Andrabi SA, Chi Z, Gagné JP, Lee Y, Ko HS, Lee BD, Poirier GG, Dawson VL, Dawson TM. Proc Natl Acad Sci U S A. 2011 Aug 23;108(34):14103-8. doi: 10.1073/pnas.1108799108. Epub 2011 Aug 8. PMID: 21825151
- PARIS (ZNF746) repression of PGC-1α contributes to neurodegeneration in Parkinson's disease. Shin JH, Ko HS, Kang H, Lee Y, Lee YI, Pletinkova O, Troconso JC, Dawson VL, Dawson TM. Cell. 2011 Mar 4;144(5):689-702. doi: 10.1016/j.cell.2011.02.010. PMID: 21376232
- Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function. Ko HS, Lee Y, Shin JH, Karuppagounder SS, Gadad BS, Koleske AJ, Pletnikova O, Troncoso JC, Dawson VL, Dawson TM. Proc Natl Acad Sci U S A. 2010 Sep 21;107(38):16691-6. doi: 10.1073/pnas.1006083107. Epub 2010 Sep 7. PMID: 20823226
Activities & Honors
- Travel Grants, 2nd World Parkinson’s Disease Congress, 2010
- Research Associate Fellowship, Hokkaido U., 2000 - 2003
- Award for President’s Outstanding Research, Association of Korean Neuroscientists (AKN), 2005
- Association of Korean Neuroscientists (AKN)
- Baltimore Life Scientists Association (BLSA)
- Korean-American Scientists and Engineers Association (KSEA)
- Society for Neuroscience (SFN)
- World Parkinson Congress (WPC)
Videos & Media
Lectures and Presentations
Mechanisms of Parkin’s Violations in Parkinson’s Disease
Baltimore, MD (03/01/2007)
Baltimore Life Scientists’ Association
New Understanding of Molecular Mechanisms in Parkinson’s Disease
Recent News Articles and Media Coverage