엄성희 교수
Sung Hee Eom
성균관대학교 의학과 · 의학
연구실 소개
엄성희 교수의 연구실은 대사 균형과 세포 에너지 신호전달 경로의 분자 기전을 중심으로 연구를 진행하고 있습니다. 특히 mTOR 및 S6K2를 통한 당 대사 조절, PPARα 활성화, 그리고 당뇨병과 관련된 베타세포 생존 메커니즘을 규명하고자 하며, 암세포의 에너지 대사 및 산성 환경 형성에 기여하는 ATP6V0C 단백질의 기능 또한 집중적으로 연구하고 있습니다. 이와 더불어, 대사 질환과 자가면역질환의 분자 기전을 밝히는 데 기여하는 신호전달 경로의 기능을 탐색하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15UNLABELLED: Nutrient homeostasis is tightly regulated by the balance between energy production and utilization. During fasting, production of ketone bodies as an alternative energy source is critical to maintain nutrient homeostasis. An important component in the nutrient-sensitive signaling pathway is S6 kinase 2 (S6K2), a downstream effector of mammalian target of rapamycin. Here, we show that mice lacking S6K2 exhibit elevated levels of ketone bodies and enhanced peroxisome proliferator-activ
Impaired nutrient sensing and dysregulated glucose homeostasis are common in diabetes. However, how nutrient-sensitive signaling components control glucose homeostasis and β cell survival under diabetic stress is not well understood. Here, we show that mice lacking the core nutrient-sensitive signaling component mammalian target of rapamycin (mTOR) in β cells exhibit reduced β cell mass and smaller islets. mTOR deficiency leads to a severe reduction in β cell survival and increased mitochondrial
These results suggest depot-specific differences in AT angiogenesis and a potential role in the susceptibility to diet-induced obesity.
The rhodium(III)‐catalyzed amidation reaction of azobenzenes with dioxazolones is described. This strategy allows the facile and efficient construction of highly substituted ortho ‐amidated azobenzenes by direct C–H cleavage approach. A wide range of substrates, excellent levels of chemoselectivity as well as high functional‐group tolerance were observed. In addition, this protocol was used to generate an array of ortho ‐amidated ketazines. Further synthetic transformation of amidated azobenzene
B-cell activating factor (BAFF) has a role in the maturation and maintenance of B cells and is associated with rheumatoid arthritis (RA). Here, we investigated whether tumor necrosis factor (TNF)-α-induced BAFF expression controls the survival of fibroblast-like synoviocytes (FLS) and whether their survival can be regulated by TNF-α-mediated upregulation of hypoxia-inducible factor (HIF)-1α using MH7A synovial cells transfected with the SV40 T antigen. More TNF-α-treated cells died compared with
The vacuolar H+-adenosine triphosphatase (ATPase) subunit V0C (ATP6V0C), a proton-conducting, pore-forming subunit of vacuolar ATPase, maintains pH homeostasis and induces organelle acidification. The intracellular and extracellular pH of cancer cells affects their growth; however, the role of ATP6V0C in highly invasive esophageal cancer cells (ECCs) remains unclear. In this study, we examined the role of ATP6V0C in glucose metabolism in ECCs. The ATP6V0C depletion attenuated ECC proliferation,
Carbamazepine is a drug that is widely used in the treatment of epilepsy and bipolar disorder. The prevalence of obesity in patients treated with carbamazepine has been frequently reported. However, whether carbamazepine affects adipogenesis, one of the critical steps in the development of obesity, remains unclear. Here, we show that carbamazepine increased the expression levels of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein β (C/EBPβ), and fatty acid syn
Type 2 diabetes mellitus (T2DM) is a worldwide heath problem that is characterized by insulin resistance and the eventual loss of β cell function. As recent studies have shown that loss of ribosomal protein (RP) S6 kinase 1 (S6K1) increases systemic insulin sensitivity, S6K1 inhibitors are being pursued as potential agents for improving insulin resistance. Here we found that S6K1 deficiency in mice also leads to decreased β cell growth, intrauterine growth restriction (IUGR), and impaired placen
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