Eunhee Kim
  • Ph. D.
  • Eunhee Kim
  • Medical Genetics
  • N11-411
  • Laboratory of Cell Signaling & Tumor Biology (N11-412)
  • +82-42-821-5495, 7542
  • eunhee@cnu.ac.kr

Academic Career

  • Ph. D., 1990, Tufts University, USA

Career

  • Senior researcher, 1990-1991, Korea Research Institute of Chemical Technology, Korea
  • Professor, 1991-2004, Pai Chai University, Korea
  • Professor, 2005-present, Chungnam National University, Korea

Research Interests

Programmed cell death is a part of the normal life cycle of many cell types and has emerged as an essential regulatory mechanism. Therefore, programmed cell death failure leads to various diseases including neurodegenerative diseases and cancer. Control of cell death can protect neurons from neurodegeneration and sensitize tumor cells to anti- cancer drug treatment. Big pharmaceutical companies put major efforts on developing cell death-regulating drugs. Thus, studying with known genes as targets would be disadvantageous for late-comers. To this end, our laboratory aims to select novel death- regulatory genes and understand their molecular mechanisms.

  • Our lab is interested in
    • Understanding molecular mechanisms of cell death
    • Pathogenesis mechanism of diseases by dysregulation of cell death
    • Drug development related such diseases
  • Current research involves
    • Identification and validation of novel death proteins as drug targets
    • Screening and optimization of small molecules targeting death proteins
    • Development of disease animal models

Selected Publication

  • Jang KH, Do YJ, Son D, Son E, Choi JS, Kim E. 2017. AIF-independent parthanatos in the pathogenesis of dry age-related macular degeneration. Cell Death Dis. 8, e2526
  • Yu C, Kim B, Kim E. 2016. FAF1 mediates regulated necrosis through PARP1 activation upon oxidative stress leading to dopaminergic neurodegeneration. Cell Death Differ. 23, 1873-85
  • Sul JW, Park MY, Shin JH, Kim YR, Yoo SE, Kong YY, Kwon KS, Lee YH, Kim E. 2013. Accumulation of the parkin substrate, FAF1, plays a key role in the dopaminergic neurodegeneration. Hum Mol Genet. 8, 1558-1573.