Lee, Chul-Hwan
Ph.D. / Associate professor
Epigenetics and Molecular Pharmacology
TEL +82-2-740-8133
FAX 02-745-7996
E-MAIL chulhwan@snu.ac.kr
WEBSITE http://chulhwanlab.com/
Research
Research Field
Our research is centered on epigenetic alterations in human diseases, especially in cancer and developmental diseases. These diseases are not only caused by DNA mutations, but also by changes in gene expression, i.e., epigenetic changes. These gene expression changes are greatly affected by histone modifications. We are currently working on following aims.1) The role of histone modifications in cardiomyocyte differentiation.
2) Epigenetic changes and epigenetic memory in pediatric glioma.
3) Epigenetic-targeted therapy in blood cancer.
Eventually, we are aiming to develop disease-specific therapy through these epigenetic studies.
Keyword
Epigenetics, histone modifications, heterochromatin, Polycomb Group proteinsEducation
- 2001-2005 B.S. KAIST, Department of Biological Sciences
- 2005-2010 Ph.D. KAIST, Department of Biological Sciences
Career
- 2011-2015 PostDoc, UTSW Medical Center
- 2015-2020 PostDoc/Research Specialist, HHMI/NYU
- 2020-Current Associate Professor, SNU Medicine, Department of Pharmacology and Biomedical Sciences
Publication
- Lee CH et al., (2019) Automethylation of PRC2 promotes H3K27 methylation and is impaired in H3K27M pediatric glioma. Genes & Development [IF=9.527] 33(19-20),1428-1440.
- Yu JR*, Lee CH* et al., (2019) PRC2 is high maintenance. Genes & Development [IF=9.527] 33(15-16), 903-935.
- Stafford JM*, Lee CH* et al., (2018) Multiple modes of PRC2 inhibition elicit global chromatin alterations in H3K27M pediatric glioma. Science Advances [IF=13.116] 4(10), eaau5935.
- Lee CH et al., (2018) Distinct stimulatory mechanisms regulate the catalytic activity of Polycomb Repressive Complex 2 (PRC2). Molecular Cell [IF=15.584] 70(3),435-448.
- Lee CH et al., (2018) Allosteric activation dictates PRC2 activity independent of its recruitment to chromatin. Molecular Cell [IF=15.584] 70(3), 422-434.
