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Younghoon  Kee

Younghoon Kee

Younghoon Kee
Associate Professor

Contact

Office: BSF 216
Phone: 813/974-5352
Lab: BSF 262, 264
Fax: 813/974-1614
Email:

Education

  • M.S. Hankuk University of Foreign Studies, South Korea (2001)
  • Ph.D. University of Texas at Austin (2006)
  • Postdoctoral Fellow. Dana-Farber Cancer Institute/Harvard Medical School (2007-2011)

Honors and Awards

2005: A.P. Bradie Endowed Golden Research Award (UT-Austin)
2006: Outstanding Teaching Award (UT-Austin)
2008-2011: Career Development Fellowship, Leukemia and Lymphoma Society
2008: Honor Award, Leukemia and Lymphoma Society Naming Program in the Field of Blood cancer Research
2014: USF New Researcher Grant
2014: USF Proposal Enhancement Grant
2014: Moffitt-American Cancer Society Institutional Grant

Research Funding (current)

2015-NIH R15
NIH RO1

Professional Memberships

  • Collaborator Member, Moffitt Cancer Center, Tampa FL
  • American Society for Biochemistry and Molecular Biology (ASBMB)
  • Korean-American Scientists and Engineers Association (KSEA)

Research

Safeguarding genomic integrity from genotoxic stresses is critical for biology of a cell. DNA repair or DNA damage responses are under sophisticated controls that must be accurately and rapidly executed, when the genome integrity is challenged. Understanding the molecular regulation of DNA damage response factors that promote genome stability is a significant subject for basic biological perspective as well as clinical aspects. Our lab studies molecular mechanisms of maintaining genome integrity, by studying the functions of proteins involved in DNA damage response and DNA repair. Below are the main areas we are currently focusing on:

1. Transcriptional silencing during DNA damage response

DNA damage response is a concerted action of numerous mechanisms that ensure to minimize genomic error. Among the mechanisms is a temporary suppression of transcription at the damaged lesions. Failure in such mechanism can compromise genomic or proteomic integrity through faulty RNA synthesis, and could lead to tumorigenesis or other disorders. BMI1, an integral component of Polycomb-Repressive Complex 1 (PRC1), is a critical factor that regulates epigenetic gene silencing during organismal development or cellular differentiation. Amplification of BMI1 is frequently observed in a various cancer types, suggesting that it has an oncogenic property when misregulated. Recent evidence also suggests that BMI1 is implicated in DNA damage response. We are studying how transcriptional silencing is regulated during DNA damage response, particularly focusing on BMI1 and its potential downstream factors that may modulate transcriptional outputs. We also study the possible roles of histone ubiquitination in gene expression regulation as well as in DNA repair.

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2. Fanconi Anemia DNA repair pathway

Fanconi Anemia (FA) is a genomic instability disorder that is associated with defective DNA repair activities. FA individuals display congenital anomaly, bone marrow disorder, and increased cancer incidence. At the cellular level, FA cells show hypersensitivity to DNA damaging agents such as Cisplatin and Mitomycin C. There are currently 19 FA subtypes (FANCA ~ FANCT) identified, whose gene products are believed to function in a common pathway that coordinate and execute DNA repair activities. Presence of such large number of protein subgroups that give rise to FA underscores the complex genetics of the disease and presents FA as an important model disease to study how DNA repair activities are executed in response to genotoxic insults. One of the underlying molecular events defective in the FA cells is monoubiquitination of FANCD2 protein by a group of nuclear FA proteins (FANC-A, B, C, E, F, G, L, and M) that function as an E3 ubiquitin ligase. The monoubiquitinated FANCD2 functionally interacts with other DNA repair proteins, such as RAD51 DNA homologous recombination (HR) repair factor, or nucleases FAN1 and CtIP, to facilitate DNA repair pathways in response to various genotoxic stresses. We are interested in understanding the regulation and function of FANCD2 monoubiquitination, as well as the functional interplay between the FA proteins and the canonical HR repair proteins.

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3. Role of deubiquitinating enzymes in DNA repair processes

The ubiquitin-proteasome system (UPS) is an essential regulatory mechanism for promoting genome stability. Deubiquitinating enzymes (DUBs), integral components of the UPS, have emerged as key players in the maintenance of the genome stability. Our lab particularly studies function and regulation of DUBs in promoting DNA repair activities in human cells.

For these projects, we use a range of modern molecular biology tools that include mammalian cell culture, RNAi, gene knockouts, confocal microscopy, and mass spectrometry analysis.

Graduate Students

Jasmin D'Andrea, Angelo De Vivo, Dawn Moody, Anthony Sanchez

Current Courses

RefCourseSecCourse TitleCRDayTimeLocation
88345BSC 4905006Independent Study
1



TBA 100

91307BSC 4910008Undergraduate Research
1



TBA 100

89438BSC 6932044Ubiquitin, DNA Damage Response
S/U Grade Consent of Instructor
1



TBA 100

85872BSC 7910040Directed Research
1-19



TBA 100