Sung Soo Chung
Seoul National University · 医学
研究室紹介
Professor Sung Soo Chung's research lab focuses on the molecular mechanisms underlying metabolic diseases, particularly insulin resistance, type 2 diabetes, and adipogenesis, with a strong emphasis on transcriptional and post-translational regulation. The lab investigates the roles of nuclear receptors (e.g., PPARγ, PPARδ), SUMOylation machinery (especially SENP2), and signaling pathways (e.g., Wnt/β-catenin) in energy metabolism and cellular differentiation. Additionally, the lab explores spinal biomechanics and clinical outcomes in lumbar total disc replacement, linking molecular regulation to orthopedic surgery and patient recovery. Their work bridges molecular biology with translational medicine, aiming to identify novel therapeutic targets for metabolic and degenerative diseases.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Oxidative stress plays an important role in the pathogenesis of insulin resistance and type 2 diabetes mellitus and in diabetic vascular complications. Thiazolidinediones (TZDs), a class of peroxisome proliferator-activated receptor gamma (PPARgamma) agonists, improve insulin sensitivity and are currently used for the treatment of type 2 diabetes mellitus. Here, we show that TZD prevents oxidative stress-induced insulin resistance in human skeletal muscle cells, as indicated by the increase in i
Here, we demonstrate that SENP2, a desumoylating enzyme, plays a critical role in the control of adipogenesis. SENP2 expression was markedly increased upon the induction of adipocyte differentiation, and this increase was dependent on protein kinase A activation. Remarkably, knockdown of SENP2 led to a dramatic attenuation of adipogenesis with a marked decrease in PPARgamma and C/EBPalpha mRNA levels. Knockdown of SENP2 also caused a marked reduction in the level of C/EBPbeta protein but not in
A lumbar total disc replacement (TDR) is believed to be a promising substitute in the surgical treatment for lumbar degenerative disc disease. The purpose of this study is to report the clinical and radiographic outcomes of 36 consecutive patients who underwent lumbar TDR using ProDisc II, and the factors associated with a better clinical outcome after a 2-year minimum follow-up. At the time of the latest follow-up, the success rate was 94% of 36 patients according to the criteria of the US Food
Small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) that reverse protein modification by SUMO are involved in the control of numerous cellular processes, including transcription, cell division, and cancer development. However, the physiological function of SENPs in energy metabolism remains unclear. Here, we investigated the role of SENP2 in fatty acid metabolism in C2C12 myotubes and in vivo. In C2C12 myotubes, treatment with saturated fatty acids, like palmitate, led to nuclear fac
Activation of the Wnt/β-catenin signaling pathway inhibits adipogenesis, while disruption of Wnt signaling leads to spontaneous adipogenesis. CCAAT/enhancer binding protein β (C/EBPβ) is rapidly induced in early stages of adipogenesis and is responsible for transcriptional induction of two major adipogenic transcription factors, peroxisome proliferator-activated receptor γ (PPARγ) and C/EBPα. In this study, we examined whether C/EBPβ is involved in the suppression of Wnt/β-catenin signaling duri
A lumbar total disc replacement (TDR) is a type of motion-preserving surgery, which aims to restore and maintain the normal range of motion (ROM) and the sagittal balance of the spine. However, little is known regarding how the spinopelvic alignment and ROM of the lumbar spine are influenced by the lumbar TDR with ProDisc. This study retrospectively analyzed the sagittal alignment and ROM of the lumbar spine in 26 consecutive patients who had undergone the TDR with ProDisc with a minimum follow-
Abnormally high levels of circulating free fatty acids can lead to pancreatic islet β-cell dysfunction and apoptosis, contributing to β-cell failure in Type 2 diabetes. The NAD+-dependent protein deacetylase Sirtuin-3 (SIRT3) has been implicated in Type 2 diabetes. In this study, we tested whether SIRT3 overexpression affects palmitate-induced β-cell dysfunction in cells of line NIT1, which are derived from mouse pancreatic β-cells. Two different lengths of SIRT3 were overexpressed: full length
PPAR (peroxisome-proliferator-activated receptor) γ, a nuclear receptor, can be conjugated with SUMO (small ubiquitin-like modifier), which results in the negative regulation of its transcriptional activity. In the present study, we tested whether de-SUMOylation of PPARγ affects the expression of PPARγ target genes in mouse muscle cells and investigated the mechanism by which de-SUMOylation increases PPARγ transcriptional activity. We found that the SUMO-specific protease SENP2 [SUMO1/sentrin/SM
>본 연구는 미국과 영국의 교장 양성(자격) 과정을 분석해 봄으로써 한국 교장 자격 제도의 바람직한 개선 방향을 모색하본 연구는 미국과 영국의 교장 양성(자격) 과정을 분석해 봄으로써 한국 교장 자격 제도의 바람직한 개선 방향을 모색하는 데 그 목적이 있다. 연구목적을 달성하기 위해, 우리나라와 달리 각 주마다 서로 다른 교장 양성 및 자격 프로그램을 실시하고 있는 미국의 사례와 우리나라와 유사하게 교장 자격을 국가에서 관리하고 있는 영국의 사례를 선정하여 분석하였다. 구체적으로, 미국의 경우, 비교적 큰 도시인 뉴욕주 콜롬비아 대학의 교장 양성프로그램(SPA)을 중심으로 캘리포니아주 UC-버클리 대학의 교장 양성 프로그램(PLI)을 비교하여 분석하였고, 영국은 영국국립교장연수원의 교장 자격 연수(NPQH)프로그램을 분석하였다. 연구 결과, 다음과 같은 시사점을 도출하였다. 첫째, 학교장으로써 지녀야할 핵심 역량에 기반하여 교장 자격 연수 내용이 구성되어야 한다. 둘째, 현행 1
Peroxisome proliferator-activated receptor gamma (PPARγ) is a critical regulator of carbohydrate and lipid metabolism, adipocyte differentiation and inflammatory response. Post-translational modification of PPARγ and its degradation involve several pathways, including the ubiquitin–proteasome system. Here, we identified F-box only protein 9 (FBXO9) as an E3 ubiquitin ligase of PPARγ. We screened interacting partners of PPARγ using immunoprecipitation and mass spectrometric analysis and identifie
Increasing evidence has shown that small ubiquitin-like modifier (SUMO) modification plays an important role in metabolic regulation. We previously demonstrated that SUMO-specific protease 2 (SENP2) is involved in lipid metabolism in skeletal muscle and adipogenesis. In this study, we investigated the function of SENP2 in pancreatic β cells by generating a β cell-specific knockout (Senp2-βKO) mouse model. Glucose tolerance and insulin secretion were significantly impaired in the Senp2-βKO mice.