경희대학교 · Medicine
Sung Soo Kim 교수의 연구실은 대사질환, 신경퇴행성질환 및 암의 분자 기전을 중심으로 세포 신호전달 경로와 세포 사멸 메커니즘을 연구하고 있습니다. 특히 인슐린 저항성, 지방세포 기능 이상, ER 스트레스 및 유전자 발현 조절을 통한 대사질환의 발달 메커니즘을 규명하고 있으며, 알츠하이머병에서의 단백질 오남열과 세포 사멸 경로, 암세포에서의 TRAIL 유도 Apoptosis 신호전달 경로의 역할도 집중적으로 연구하고 있습니다. 이들의 연구는 질병의 조기 진단 및 타겟 치료 전략 개발에 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Metabolic disorders, including type 2 diabetes (T2DM) and cardiovascular disease (CVD), present an increasing public health concern and can significantly undermine an individual's quality of life. The relative risk of CVD, the primary cause of death in T2DM patients, is two to four times higher in people with T2DM compared with those who are non-diabetic. The prevalence of metabolic disorders has been associated with dynamic changes in dietary macronutrient intake and lifestyle changes over rece
Alzheimer's disease (AD) is characterized by the deposition of aggregated beta-amyloid (Abeta), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of ER stress-mediated Abeta neuro
Prepregnancy obesity is associated with increased risks of a wide range of adverse pregnancy and neonatal outcomes among women without chronic diseases.
To determine the apoptotic signaling pathway which tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) induced, we investigated the contribution of reactive oxygen species (ROS), p38 mitogen-activated protein (MAP) kinase and caspases in human adenocarcinoma HeLa cells. Here we show that upon TRAIL/Apo2L exposure there was pronounced ROS accumulation and activation of p38 MAP kinase, and that activation of caspases and apoptosis followed. Pretreatment with antioxidants such as
