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Training
- B.Sc., 1977: Seoul National University, Korea
- M.Sc., 1980: Korea Advanced Institute of Science, Korea
- Ph.D., 1987: University of Texas, Austin, Texas
- Post-Doctoral, 1991: Sloan-Kettering Cancer Institute, New York
Positions
- Professor, 2002-present: Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis,IN
- Member, 2002-present: Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN
- Member, 2002-present: Indiana University Cancer Center, Indiana University School of Medicine, Indianapolis, IN
- Associate Professor, 1997-2002: Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN
- Associate Member, 1997-2002: Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN
- Member, 1997-2002: Indiana University Cancer Center, Indiana University School of Medicine, Indianapolis, IN
- Adjunct Faculty, 1993-1997: University of Tennessee College of Medicine, Dept of Pathology, Memphis, TN
- Assistant Member, 1992-1997: Dept of Virology & Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN
- Research Associate, 1987-1991: Molecular Biology, Sloan-Kettering Cancer Center, New York, NY
 Summary of the focus of the research of Dr. Lee
DNA damage due to irradiation or chemicals must be repaired to prevent gene alterations that could give rise to cancer. Our objective is to understand the molecular mechanism of DNA damage and repair using gene, cell and animal models . In addition, we are targeting several DNA repair factors as a means to sensitize cancer cells to DNA damaging agents.
Description and summary of research focus of the laboratory:
DNA damage due to UV-irradiation, ionizing radiation, or chemicals must be repaired to prevent genomic alterations that could otherwise give rise to cancer. For this reason, cells invoke various mechanisms to repair their DNA and to prevent DNA replication until the damage is repaired. Our long-term objective is to understand the molecular mechanism of how DNA damage induces S-phase (or replication) arrest. To meet this objective, our research focuses on (1) identifying and characterizing genes involved in DNA damage-signaling pathway, (2) defining the molecular mechanism of damage-induced replication arrest, and (3) initiation of damaged DNA repair. Combination of genetic and biochemical approaches has been used to identify genes involved in replication arrest following DNA damage. We are trying to identify potential target proteins (human replication protein A, simian virus 40 large T-antigen) involved in the regulation of DNA replication. In order to understand DNA damage signaling pathway, mutant cells lacking DNA-dependent protein kinase (DNA-PKcs), p53, p21cip1waf1, ataxia telangiectasia mutated (ATM), and fanconi anemia genes are being analyzed for their roles in damage-induced replication arrest. Our recent study indicates that DNA-PK plays an essential role in damage-induced replication arrest. Current effort to identify target protein(s) for DNA-PK is underway.
Recognition of damaged DNA is also an integral part of damage-induced S-phase arrest. Xeroderma pigmentosum complementation group A (XPA), XPC, TFIIH, and RPA are all involved in recognition of intrastrand damaged DNA, whereas initiation of interstrand cross-link repair is still unknown. We employ state-of-the-art technology to carry out interaction between repair proteins and inter- or intra-strand DNA damage.
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