Dr Jin Young Kim (金眞英博士)

PhD (Rutgers University – Robert Wood Johnson Medical School)

Assistant Professor

Dr Jin Young Kim

Contact Information

Office: 1B-208, 2/F, Block 1,
To Yuen Building
Phone: +852 3442-4309
Fax: +852 3442-0549
Email: jinyoung.kim@cityu.edu.hk
Web: CityU Scholars

Research Interests

  • Neurons and Glial Cells
  • Circadian Clocks
  • Neurodegeneration
  • Regeneration

Dr Kim received her M.S. degree at SungKyunKwan University in South Korea, where she studied the role of aminoacyl-tRNA synthetase complex under the mentoring of Prof. Sunghoon Kim. Then, she moved to USA for her next step and obtained PhD degree from Department of Neuroscience and Cell Biology at Rutgers University in 2009. During this period, she discovered the novel mechanism of neurodegeneration under the guidance of Prof. Patrizia Casaccia, and her work was featured in several leading journals because of its new perspectives in the field. In 2010, she joined Prof. Charles J. Weitz lab in Department of Neurobiology at Harvard Medical School for her postdoctoral training. Her work about the regulatory mechanism of circadian clocks was also highlighted. In September 2015, she joined the Department of Biomedical Sciences at City University of Hong Kong as an assistant professor.

Research Interest

Circadian clocks are endogenous oscillators to generate daily biological rhythms in metabolism, behavior, and physiology. A growing body of evidence has shown the abnormal circadian rhythms such as altered sleep and dysregulation of hormone levels in patients with the central nervous system (CNS) disorders. However, little is known about what the underlying mechanisms are. Our missions are understanding physiological functions of circadian clocks in the CNS cells (i.e., neurons and glial cells) and the effects of altered circadian clocks on the CNS disorders including neurodegenerative diseases. The ultimate goal is to find novel therapeutic targets and design advanced treatment strategies based on circadian cycles.

In the molecular level, the core of mammalian circadian clocks is a transcriptional negative feedback loop, highly conserved from the brain to all peripheral tissues. This feedback loop also drives daily rhythmic expression of thousands of genes involved in diverse cellular processes and signaling pathways. We use biochemical and molecular biological approaches to investigate molecular mechanisms of neurodegeneration affected by circadian clocks, and vice versa. The research in our lab is performed with in vitro (primary cultures), ex vivo (brain slice cultures), and in vivo (animal models) systems.

Current Research Interests

  1. What are circadian genes expressed in neurons and/or glial cells?
  2. How do circadian clocks regulate neuronal and glial physiology through transcriptional regulation of circadian genes?
  3. How are circadian clocks involved in neurodegeneration: a cause or a consequence?
  4. Reversibility, therapeutic targets, and treatment strategies of neurodegenerative diseases

Publications

  1. Jin Young Kim, Pieter Bas Kwak, Michael Gebert, Hao A. Duong, Charles J. Weitz. Purification and Analysis of PERIOD Protein Complexes of the Mammalian Circadian Clock. Methods in Enzymology, Vol. 551:197-210, 2015
  2. Jin Young Kim, Pieter Bas Kwak, Charles J. Weitz. Specificity in Circadian Clock Feedback from Targeted Reconstitution of the NuRD Corepressor. Molecular Cell, 56 (6): 738-748, 2014

    This paper has been featured in:

    • Research Highlight, in brief: Andrea Du Toit. NuRD sets the CLOCK. Nature Reviews Molecular Cell Biology 16 (2), 2015
  3. Laura Lande-Diner*, Cyril Boyault*, Jin Young Kim, and Charles J. Weitz. A positive feedback loop links circadian clock factor CLOCK-BMAL1 to the basic transcriptional machinery. Proc. Natl. Acad. Sci. USA, 110(40): 16021-6, 2013 (*Contributed equally)
  4. Ye He, Jin Young Kim, Jeffrey Dupree, Ambika Tewari, Carmen Melendez-Vasquez, John Svaren, Patrizia Casaccia. YY1 as molecular link between neuregulin and transcriptional modulation of peripheral myelination. Nature Neuroscience, 13 (12): 1472-1480, 2010
  5. Jin Young Kim and Patrizia Casaccia. HDAC1 in axonal degeneration: a matter of subcellular localization. Cell Cycle, 9 (18): 3680-3684, 2010 (Extra-Views)
  6. Jin Young Kim, Siming Shen, Karen Dietz, Ye He, Owain Hawell, Richard Reynolds, Patrizia Casaccia. HDAC1 nuclear export induced by pathological conditions is essential for the onset of axonal damage. Nature Neuroscience, 13 (2):180-189, 2010 (as the cover article)

    This paper has been featured in:

    • News and Views: Robert H Miller. Renegade nuclear enzymes disrupt axonal integrity. Nature Neuroscience 13 (2): 143-144, 2010
    • Research Highlight: Leonie Welberg. Neurodegeneration: Export disrupts transport. Nature Reviews Neuroscience 11, February 2010
    • Evaluations:
      Charlotte Teunissen. Faculty of 1000 Medicine 27 January 2010
      Scott Russo and Eric Nestler. Faculty of 1000 Medicine 05 March 2010
  7. Jin Young Kim and Patrizia Casaccia-Bonnefil. Interplay of hormones and p53 in modulating gender dimorphism of subventricular zone cell number. Journal of Neuroscience Research, 87:3297-3305, 2009
  8. Jiadong Li, Cristina A. Ghiani, Jin Young Kim, Aixiao Liu, Juan Sandoval, Jean DeVellis, Patrizia Casaccia-Bonnefil. Inhibition of p53 transcriptional activity: a potential target for future development of therapeutic strategies for primary demyelination. Journal of Neuroscience, 28:6118-6127, 2008
  9. Jung Min Han, Sang Gyu Park, Bei Liu, Bum-Joon Park, Jin Young Kim, Cheng He Jin, Yeong Wook Song, Zihai Li and Sunghoon Kim. Aminoacyl-tRNA Synthetase-Interacting Multifunctional Protein 1/p43 controls endoplasmic reticulum retention of heat shock protein gp96: Its pathological implications for lupus-like autoimmune disease. American Journal of Pathology, 170:2042-2054, 2007
  10. Sang Gyu Park, Young Sun Kang, Jin Young Kim, Chang Seok Lee, Young Gyu Ko, Woo Je Lee, Ki-Up Lee, Young Il Yeom and Sunghoon Kim. Hormonal activity of AIMP1p43 for glucose homeostasis. Proc. Natl. Acad. Sci. USA, 103:14913-14918, 2006
  11. Jung Min Han, Jin Young Kim, and Sunghoon Kim. Molecular network and functional implications of macromolecular tRNA synthetase complex. Biochemical and Biophysical Research Communication, 303:985-993, 2003, Review
  12. Jin Young Kim, Young-Sun Kang, Jung-Won Lee, Hyoung June Kim, Young Ha Ahn, Heonyong Park, Young-Gyu Ko, and Sunghoon Kim. p38 is essential for the assembly and stability of macromsolecular tRNA synthetase complex: Implications for its physiological significance. Proc. Natl. Acad. Sci USA, 99:7912-7916, 2002
  13. Young-Gyu Ko, Young-Sun Kang, Heunyong Park, Wongi Seol, Jin Young Kim, Taeho Kim, Hee-Sae Park, Eui-Ju Choi, and Sunghoon Kim. Apoptosis Signal-regulating Kinase Controls the Proapoptotic Function of Death-associated Protein (Daxx) in the Cytoplasm. J. Biol. Chem., 276:39103-39106, 2001