Sung Hee Eom
Sungkyunkwan University · 医学
研究室紹介
Professor Sung Hee Eom's research lab focuses on cellular metabolism, nutrient sensing signaling pathways, and their roles in metabolic diseases such as diabetes and obesity. The lab investigates key regulators like mTOR, S6K2, and PPARα in maintaining glucose and energy homeostasis, particularly under metabolic stress. It also explores the role of ion transporters like ATP6V0C in cancer cell metabolism and tumor progression, especially in esophageal cancer. Additionally, the lab examines the interplay between inflammatory signaling, hypoxia, and cell survival in autoimmune and metabolic disorders.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
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