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Han Seok Ko, Ph.D., M.S.

Headshot of Han Seok Ko
  • Associate Professor of Neurology

Research Interests

Molecular and Cellular Signals Controlling Neurodegeneration; Parkinson's disease more


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:

  1. Mechanisms of neurodegeneration in human alpha-synuclein transgenic mice.
  2. The interaction between Glucocerebrosidase (GBA) and Parkinson’s disease.
  3. Identification and characterization of important pathophysiologic substrates of parkin that link parkin function to familial and sporadic PD. more


  • Associate Professor of Neurology

Departments / Divisions

Centers & Institutes



  • Ph.D.; Hokkaido University (Japan) (2003)
  • B.S.; Konkuk University (Korea) (1998)
  • M.S.; Konkuk University (Korea) (2000)

Additional Training

  • The Johns Hopkins School of Medicine, Baltimore, MD, 2008, Neurobiology

Research & Publications

Research Summary

Molecular mechanisms driving the loss of brain cells in Parkinson’s disease patients.

Selected Publications

View all on PubMed

Ko HS, Lee Y, Shin JH, Karuppagounder SS, Gadad BS, Koleske AJ, Pletnikova O, Troncoso JC, Dawson VL, Dawson TM. Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function. Proc. Natl. Acad. Sci. U.S.A. 2010;107(38):16691-16696

Shin JH, Ko HS, Kang H, Lee Y, Lee YI, Pletinkova O, Troconso JC, Dawson VL, Dawson TM. PARIS (ZNF746) Repression of PGC-1alpha Contributes to Neurodegeneration in Parkinson's Disease. Cell. 2011;144(5):689-702

Karuppagounder SS, Brahmachari S, Lee Y, Dawson VL, Dawson TM*, Ko HS*. The c-Abl inhibitor, nilotinib, protects dopaminergic neurons in a preclinical animal model of Parkinson's disease. Sci Rep. 2014; 4:4874. * Co-corresponding author

Brahmachari S, Ge P, Lee SH, Kim D, Karuppagounder SS, Kumar M, Mao X, Shin JH, Lee Y, Pletnikova O, Troncoso JC, Dawson VL, Dawson TM*, Ko HS*. Activation of tyrosine kinase c-Abl contributes to α-synuclein-induced neurodegeneration. J Clin Invest. 2016;126(8):2970-88. *Co-corresponding author

Mao X, Ou MT, Karuppagounder SS, Kam TI, Yin X, Xiong Y, Ge P, Umanah GE, Brahmachari S, Shin JH, Kang HC, Zhang J, Xu J, Chen R, Park H, Andrabi SA, Kang SU, Gonçalves RA, Liang Y, Zhang S, Qi C, Lam S, Keiler JA, Tyson J, Kim D, Panicker N, Yun SP, Workman CJ, Vignali DA, Dawson VL*, Ko HS*, Dawson TM*. Pathological α-synuclein transmission initiated by binding lymphocyte-activation gene 3. Science. 2016;353(6307). *Co-corresponding author. Recommended by F1000 prime


Transcriptional repression leading to parkinson's disease
Patent # US9274128 B2 | 

Parkinson's disease is caused by the preferential loss of substantia nigra dopamine neurons. A Parkin Interacting Substrate, PARIS (ZNF746) is identified. The levels of PARIS are regulated by the ubiquitin proteasome system via binding to and ubiquitination by the E3 ubiquitin ligase, parkin. PARIS is a KRAB and zinc finger protein that accumulates in models of parkin inactivation and in human brain Parkinson's disease patients. PARIS represses the expression of the transcriptional co-activator, PGC-1α and the PGC-1α target gene, NRF-1 by binding to insulin response sequences in the PGC-1α promoter. Conditional knockout of parkin in adult animals leads to progressive loss of dopamine (DA) neurons that is PARIS dependent. Overexpression of PARIS causes selective loss of DA neurons in the substantia nigra, which is reversed by either parkin or PGC-1α co-expression. The identification of PARIS provides a molecular mechanism for neurodegeneration due to parkin inactivation.

Contact for Research Inquiries

Email me Phone: 410-502-5454

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
  • AKN Jr Faculty Award, Association of Korean Neuroscientists
  • Maryland Innovation Initiative (MII) Award, TEDCO
  • Discovery fund Innovation Award, JHU
  • Discovery Innovation Award, The Johns Hopkins University School of Medicine, 2017


  • Association of Korean Neuroscientists (AKN), Council Member
  • Baltimore Life Scientists Association (BLSA)
  • Korean-American Scientists and Engineers Association (KSEA)
  • Society for Neuroscience (SFN)

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
    Singapore (04/01/2009)
  • LAG3 mediates cell-to-cell transmission of -synuclein pathology
    Oral, UKC
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