Kyu Hyuck Chung
성균관대학교 약학대학 · 의학
Kyu Hyuck Chung 교수의 연구실은 주로 간 섬유화, 폐 섬유화 및 미세플라스틱의 생체 독성 메커니즘을 중심으로 한 약리학적·분자생물학적 연구를 수행하고 있습니다. 특히, 자연물에서 유래한 신질소 화합물과 미세플라스틱의 세포 및 유전자 수준에서의 독성 영향을 규명하며, 섬유화 억제 및 항염증 작용을 가진 신약 후보 물질의 개발에 초점을 맞추고 있습니다. RNA 간섭 기반 유전자 기능 분석 기술의 개발을 통해 분자 생물학적 기법의 응용도 함께 확장하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Vector-based RNA interference (RNAi) has emerged as a valuable tool for analysis of gene function. We have developed new RNA polymerase II expression vectors for RNAi, designated SIBR vectors, based upon the non-coding RNA BIC. BIC contains the miR-155 microRNA (miRNA) precursor, and we find that expression of a short region of the third exon of mouse BIC is sufficient to produce miR-155 in mammalian cells. The SIBR vectors use a modified miR-155 precursor stem-loop and flanking BIC sequences to
The detection of high levels of microplastics in indoor and outdoor air has increased concerns regarding its toxic effects on the respiratory system. They are not easily degradable and can be deposited deep in the lungs. Although several studies have reported inhalation toxicities of microplastics, they are still controversial due to a lack of evidence. Herein, we evaluated the inhalation toxicities of three differently charged polystyrene microplastics (PS-MPs), the most abundant microplastics
Abstracts <b>Objective:</b> The major active ingredient of humidifier disinfectant, polyhexamethylene guanidine-phosphate (PHMG-P), caused hundreds of deaths with pulmonary fibrosis. However, structurally similar guanidine-based disinfectants are still in use in various fields. Moreover, as they are precursors of excellent antimicrobial compounds, new chemicals with guanidine-based structures have been synthesized and introduced. In this study, we evaluated pulmonary fibrotic responses induced b
Hepatic fibrosis is characterized by the abnormal deposition of extracellular matrix (ECM) proteins. During hepatic fibrogenesis, hepatic stellate cell (HSC) activation followed by chronic injuries is considered a key event in fibrogenesis, and activated HSCs are known to comprise approximately 90% of ECM-producing myofibroblasts. Here, we demonstrated that (-)-catechin-7-<i>O</i>-β-d-apiofuranoside (C7A) significantly inhibited HSC activation via blocking the signal transducer and activator of