Quality Control University

Seokwon Kang

Biochemistry and Molecular Biology

Kimmel Cancer Center

Thomas Jefferson University

*** *. **** ******, ************, PA 19107

Tel: 215-***-****

E-mail: hvrmfb@r.postjobfree.com

Education

Mar. 99-Feb. 05 Seoul National University College of Medicine, South Korea

Ph.D. in Cancer Biology

Thesis: Inactivation of p38 kinase delays the onset of senescence in rabbit articular chondrocytes

Overall GPA: 3.62/4.30

Mar. 95-Feb. 97 Sogang University, South Korea

M.S. in Biology

Thesis: Characterization of human rotavirus outer capsid protein VP4 from Korean patient

Overall GPA: 3.71/4.30

Mar. 91-Feb. 95 Kyunghee University, South Korea.

B.S. in Genetic Engineering

Overall GPA: 3.71/4.50

Skills

Molecular biology:

Long PCR for mitochondrial deletion. RT-PCR, cloning, DNA/RNA isolation, DNA sequencing, Southern/Northern blot.

Biochemistry:

Western blot, In vitro kinase assay, In vitro phosphatase assay, in vitro translation, Immunoprecipitaion, EMSA, Telomere length assay, TRAP assay, NO assay, ROS assay, Caspase assay, Protein expression and purification.

Cell biology:

Primary cell culture, FACS, Immunohistochemical staining, Confocal microscopy, Gene transfer (by using calcium, liposome, retrovirus/adenovirus vector system), Proliferation assay, Reporter assay, RNA interference.

Immunology:

Cell sorting, Immunization, ELISA.

Clinical experiments:

Small animal works including genotyping and phenotyping, husbandry, primary cell culture (bone marrow macrophage, splenocytes and thymocytes). Laser capture of single cell and gene analysis.

Experience

Nov. 06 – present

Biochemistry and Molecular Biology

Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107

Feb. 06 – Oct. 06

School of Molecular Biosciences

Biomolecualr X-Ray Crystallography Center, Washington State University, Pullman, WA 99163

Mar. 05 – Dec. 05

Cutaneous Research Center

Seoul National University College of Medicine, South Korea

Mar. 01 – Feb. 05

National Research Laboratory for Cell Cycle Control

Cancer Research Institute, Seoul National University College of Medicine, South Korea

Mar. 99 – Feb. 01

Laboratory of Tumor Immunology

Cancer Research Institute, Seoul National University College of Medicine, South Korea

Mar. 97 – Feb. 99

Laboratory for Slow virus

Life Science Research Institute, Hallym University College of Medicine, South Korea

Publication

Jung MS, Jin DH, Chae HD, Kang S, Kim SC, Bang YJ, Choi TS, Choi KS, Shin DY. Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing ROS-dependent p38 activation. J. Biol. Chem. 2004, 279:177**-*****

Kang S, Jung MS, Kim CW, Shin DY. Inactivation of p38 kinase delays the onset of senescence in rabbit articular chondrocytes. Mech. Ageing. Dev. 2005, 126:591-597

Li WH, Lee YM, Kim JY, Kang S, Kim S, Kim KH, Park CH, Chung JH. Transient Receptor Potential Vanilloid-1 Mediates Heat-Shock-Induced Matrix Metalloproteinase-1 Expression in Human Epidermal Keratinocyte. J. Invest. Dermatol. 2007, 127:2328-35

Fernandes-Alnemri T, Yu JW, Juliana C, Solorzano L, Kang S, Wu J, Datta P, McCormick M, Huang L, McDermott E, Eisenlohr L, Landel CP, Alnemri ES. The AIM2 inflammasome is critical for innate immunity to Francisella tularensis. Nat Immunol. 2010,11(5):385-93.

Seokwon Kang, J.P Loubutin, Pinaki Datta, David Strasser, Teresa Fernandes-Alnemri and Emad S. Alnemri. Loss of Omi/HtrA2 activity in non-neuronal tissues of adult mice causes premature aging. (Submitted). Cell Death. Differ. 2012

Abstract of Postdoctoral work

mnd2 mice die prematurely as a result of neurodegeneration at age 30-40 days after birth, due to loss of the enzymatic activity of the mitochondrial quality control protease HtrA2/Omi. Here we show that transgenic expression of HtrA2/Omi in the central nervous system of mnd2 mice rescues them from neurodegeneration and prevents their premature death. Unexpectedly, adult transgenic mnd2 mice develop accelerated aging phenotypes, such as premature weight loss, hair loss, reductions in fertility, curvature of the spine, heart enlargement, increased autophagy, and death by 12-18 months of age. These mice also have elevated levels of clonally expanded mitochondrial DNA (mtDNA) deletions in their tissues. Analyzing mitochondrial DNA (mtDNA) by PCR in COX-negative heart myofibers isolated by laser capture microdissection, I demonstrated that these mice have elevated levels of clonally expanded mitochondrial mtDNA deletions in their tissues, providing direct genetic evidence linking mitochondial protein quality control to mtDNA deletions and aging in mammals.

Abstract of Ph.D. work

Cellular senescence is a state of irreversible growth arrest shown by normal cells in culture which undergo a limited number of population doublings (PD). While tumor-derived cells show an infinite proliferation, the life span of normal cells is finite. The late stage of normal cells is characterized by an decline in proliferative potential and the establishment of a viable, nondividing population that is defined as replicative senescent cells. Generally, it has been supposed that replicative senescence is caused by telomere shortening. But other conditions, including inappropriate culture condition, also induce senescence without telomere shortening. Recently, other groups and we reported that p38 kinase plays a key role on the onset of senescence. Therefore, we hypothesized that cellular senescence in primary rabbit articular chondrocytes are due in part to growth inhibitory effects mediated by the p38. In this study, we have found that the stress-activated mitogen-activated protein kinase (MAPK), p38, is activated during the progression of senescence. Blockade of p38 activity with the chemical inhibitor SB203580 increased the cell growth rate and extended life span about two folds in contrast with control, but only when treated before the cellular commitment to senescence, implying that p38 kinase plays important roles in chondrocyte senescence induction. In addition, the expression of a dominant negative form of MKK6 (MKK6A) and p38 (DNp38) in early passage of chondrocytes effect on senescence delay. Furthermore, we demonstrated that rabbit chondrocyte senescence is independent of telomere shortening.

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