정성수 교수
Sung Soo Chung
서울대학교 · 의학
연구실 소개
정성수 교수의 연구실은 대사질환, 특히 인슐린 저항성과 제2형 당뇨병의 발병 메커니즘을 중심으로 산화 스트레스와 전사 인자, 단백질 수식화 조절을 통한 대사 조절 메커니즘을 규명하고 있습니다. 특히 PPARγ 수용체 활성화와 SENP2를 통한 단백질 디수모일화 조절이 지방세포 형성과 인슐린 민감도에 미치는 영향을 집중적으로 연구하고 있으며, 류마티스성 질환 및 척추디스크 질환의 수술적 치료 결과와도 연계된 임상적 응용 연구를 병행하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
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
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.
Thiazolidinediones (TZDs) are synthetic ligands of peroxisome proliferator-activated receptor-γ (PPARγ), a member of the nuclear receptor superfamily. TZDs are known to increase insulin sensitivity and also to have an antioxidative effect. In this study, we tested whether TZDs protect pancreatic β-cells from oxidative stress, and we investigated the mechanism involved in this process. To generate oxidative stress in pancreatic β-cells (INS-1 and βTC3) or isolated islets, glucose oxidase was adde
대표 연구 분야
정성수 교수의 연구를 Nubint에서 더 깊이 살펴보세요
이 연구실의 논문을 앱에서 열어 AI와 함께 읽고, 핵심을 요약하고, 내 글에 인용하세요.