Kim Mi Sun
Kyung Hee University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Kim Mi Sun's research lab focuses on molecular mechanisms underlying drug resistance in cancer, particularly in non-small cell lung cancer (NSCLC), with a strong emphasis on EGFR tyrosine kinase inhibitor resistance and the role of signaling pathways such as IL-6R/JAK1/STAT3. The lab also investigates key signaling cascades in immune cells, including mTORC1 activation in mast cells downstream of FcεRI and Kit receptors, and explores nuclear receptor-mediated gene regulation, particularly the liganded vitamin D receptor's role in transcriptional repression. Additionally, the lab contributes to clinical oncology and radiology by developing predictive models for breast cancer using advanced statistical methods and medical imaging data. These interdisciplinary efforts span molecular oncology, signal transduction, and translational biomedical research.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15BACKGROUND: Deletion of large blocks of nonessential genes that are not needed for metabolic pathways of interest can reduce the production of unwanted by-products, increase genome stability, and streamline metabolism without physiological compromise. Researchers have recently constructed a reduced-genome Escherichia coli strain MDS42 that lacks 14.3% of its chromosome. RESULTS: Here we describe the reengineering of the MDS42 genome to increase the production of the essential amino acid L-threon
Little is known about the signals downstream of PI3K which regulate mast cell homeostasis and function following FcepsilonRI aggregation and Kit ligation. In this study, we investigated the role of the mammalian target of rapamycin complex 1 (mTORC1) pathway in these responses. In human and mouse mast cells, stimulation via FcepsilonRI or Kit resulted in a marked PI3K-dependent activation of the mTORC1 pathway, as revealed by the wortmannin-sensitive sequential phosphorylation of tuberin, mTOR,
Although transactivation by the liganded vitamin D receptor (VDR) is well described at the molecular level, the precise molecular mechanism of negative regulation by the liganded VDR remains to be elucidated. We have previously reported a novel class of negative vitamin D response element (nVDRE) called 1alphanVDRE in the human 25(OH)D31alpha-hydroxylase [1alpha(OH)ase] gene by 1alpha,25(OH)2D3-bound VDR. This element was composed of two E-box-type motifs that bound to VDIR for transactivation,
Nursing professionals, managers and health policy makers need to understand the factors influencing depressive symptoms and to use appropriate interventions based on the severity and not just the onset.
Alzheimer's disease is a chronic neurodegenerative disorder characterized by progressive dementia and deterioration of cognitive function. Although several drugs currently used for the treatment of Alzheimer's disease delay its onset and slow its progression, still there is no drug with profound disease-modifying effects. Studies aiming the treatment of this neurodegenerative disorder explore various disease mechanisms. Since antiquity, medicinal herbs have been used in traditional medicine. Rec
The tumor suppressor genes p53, Rb, and DCC were studied in five human oral cancer cell lines (FaDu, SCC-4, HEp-2, 1483, and OEC-M1) and in primary normal human oral keratinocytes (NHOK). All tested cancer lines had similar amount of p53 messages to normal cells, but the cancer lines FaDu and SCC-4 contained significantly higher p53 protein levels than did the normal counterpart. Sequencing p53 cDNA for these cancer cells showed point mutations: In the FaDu cell line, a mutation of CGG to CTG oc