노재석 교수
Jaeseok No
연세대학교 생화학과 · 의학
연구실 소개
노재석 교수의 연구실은 에피igenetics와 세포 사멸 유도 메커니즘을 중심으로 암 치료 신약 개발을 목표로 하고 있습니다. 히스톤 변형 조절 단백질인 히스톤 락신 디메틸라제(KDM)의 기능과 작용 기전을 규명하며 암의 발생 및 유지 메커니즘을 밝혀내고, 해양 유래 화합물인 캐리스폰지올라이드가 미토콘드리아 기능을 손상시켜 세포 사멸을 유도하는 새로운 사멸 경로를 규명하고 있습니다. 특히, 자율신경계와 스트레스 호르몬이 뇌의 페달 시스템에 미치는 영향을 분석함으로써 직업적 스트레스와 뇌 구조 변화 간의 연관성도 탐구하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
4Epigenetic regulators, known as “writers,” erasers,” and “readers,” are essential for controlling gene expression by adding, removing, or recognizing post-translational modifications to histone tails, respectively. These regulators significantly affect genes involved in cancer initiation and maintenance. Recently, several clinical strategies targeting these epigenetic enzymes have emerged and some trials have demonstrated promising results for cancer treatment. Histone lysine demethylases (KDMs)
No accurate method to detect thyroid microsomal (MC) antibody (Ab) in serum has been generalized. In this study, the titer of MC Ab obtained by the method of MC autoantibody particle agglutination (MCPA) was analyzed by enzyme linked immunosorbent assay (ELISA). MC and thyroglobulin (Tg) were prepared from Graves' thyroid. ELISA was done by coating the plate with MC, adding Tg to buffer and using peroxidase-conjugated anti-h IgG. 1) The titer of MCPA correlated with the MC Ab ELISA index in seru
TPS 792: Occupational health 2, Exhibition Hall, Ground floor, August 27, 2019, 3:00 PM - 4:30 PM Introduction: The limbic system is an anatomical structure that plays a pivotal role in motivation, emotion, learning and memory. Firefighters are chronically exposed to violence, trauma and other threats. They are also constantly exposed to a variety of environmental hazardous substances. This study focused on the association of limbic system atrophy and salivary cortisone known as stress hormone.
Callyspongiolide is a marine macrolide known to induce caspaseindependent cancer cell death. While its toxic effects have been known, the mechanism leading to cell death is yet to be identified. We report that Callyspongiolide R form at C-21 (cally2R) causes mitochondrial dysfunction by inhibiting mitochondrial complex I or II, leading to a disruption of mitochondrial membrane potential and a deprivation of cellular energy. Subsequently, we observed, using electron microscopy, a drastic formatio
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