Dongmin Kang
이화여자대학교 생명과학과 · 생화학·유전·분자생물학
Dongmin Kang 교수의 연구실은 세포 신호전달, 세포주기 조절 및 산화 스트레스 반응을 중심으로 한 분자세포생물학을 연구합니다. 특히 체크포인트 단백질 Chfr의 유비퀴틴 리가제 활성과 세포주기 정류 기전, 히드록시퍼옥시드의 신호전달 기능, 그리고 자가포식(autophagy)의 분자 기전에 대한 기초 연구를 진행하고 있습니다. 또한, 구리 이온을 탐지할 수 있는 새로운 화학센서 개발을 통해 세포 내 금속 이온 모니터링 기술에도 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The checkpoint protein Chfr delays entry into mitosis, in the presence of mitotic stress (Scolnick, D.M., and T.D. Halazonetis. 2000. Nature. 406:430-435). We show here that Chfr is a ubiquitin ligase, both in vitro and in vivo. When transfected into HEK293T cells, Myc-Chfr promotes the formation of high molecular weight ubiquitin conjugates. The ring finger domain in Chfr is required for the ligase activity; this domain auto-ubiquitinates, and mutations of conserved residues in this domain abol
Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) is an oxidizing agent that induces cellular damage at inappropriate concentrations and gives rise to an arrest during cell cycle progression, causing cell death. Recent evidence indicates that H<sub>2</sub>O<sub>2</sub> also acts as a promoter for cell cycle progression by oxidizing specific thiol proteins. The intracellular concentration of H<sub>2</sub>O<sub>2</sub> is regulated tightly, enabling its use as a cellular signaling molecule while mini
Signaling by the hedgehog (hh)-class gene pathway is essential for embryogenesis in organisms ranging from Drosophila to human. We have isolated a hh homolog (Hro-hh) from a lophotrochozoan species, the glossiphoniid leech, Helobdella robusta, and examined its expression by reverse transcription polymerase chain reaction (RT-PCR) and whole-mount in situ hybridization. The peak of Hro-hh expression occurs during organogenesis (stages 10-11). No patterned expression was detected within the segment
As an intracellular degradation system, autophagy is an essential and defensive cellular program required for cell survival and cellular metabolic homeostasis in response to various stresses, such as nutrient deprivation and the accumulation of damaged organelles. In general, autophagy flux consists of four steps: (1) initiation (formation of phagophore), (2) maturation and completion of autophagosome, (3) fusion of autophagosomes with lysosomes (formation of autolysosome), and (4) degradation o
Abstract Fluorescein‐functionalized silica nanoparticles ( 1 ) were prepared by sol–gel reaction, and their optical sensing abilities were studied towards finding a new type of synthetic fluorogenic chemosensor for imaging Cu 2+ ions in living cells. Interestingly, upon addition of Cu 2+ in a H 2 O suspension of 1 at pH 7.4, 1 displays large chelation‐enhanced quenching (CHEQ) effects with Cu 2+ . With the exception of Cu 2+ , no significant fluorescence intensity changes were observed in the ex
A new fluoro-chromogenic chemosensor based on BODIPY-functionalized gold nanoparticles 1 is prepared. Addition of Cu(2+) ions to aqueous solutions of 1 gave an instantaneous color change along with a blue-shift of the absorption band and quenching of the emission spectrum at room temperature. The chemosensor 1 exhibits a high affinity and selectivity for Cu(2+) over competing metal ions tested. Moreover, confocal microscopy experiments establish that 1 can be used for detecting Cu(2+) levels wit
The chemical instability of line patterned Ge2Sb2Te5 was studied by transmission electron microscopy after electrically inducing melt and solidification. Compositional analysis showed elemental separation of Te to the anode side, while Ge and Sb mutually separated at the cathode side. Such elemental separation of Ge2Sb2Te5 is explained by the electric field effects and thermodynamic driving forces.
The zinc tank: A new fluoro-chromogenic chemosensor based on BODIPY-functionalized Fe(3)O(4) nanoparticles (1) has been prepared. Chemoprobe 1 exhibits high selectivity for Zn(2+) over other competing metal ions tested. Moreover, confocal microscopy experiments established that 1 can be used for detecting Zn(2+) levels in living cells (see figure).
Diclofenac, a nonsteroidal anti-inflammatory drug (NSAID) used to treat inflammatory diseases induces cellular toxicity by increasing the production of reactive oxygen species (ROS) and impairing autophagic flux. In this study, we investigated whether diclofenac induces cancer cell death and the mechanism by which diclofenac causes cell death. We observed that diclofenac induces mitotic arrest with a half-maximal effective concentration of 170 μM and cell death with a half-maximal lethal dose of
