Hyewon Shin

Chang Jun Lee

Hojun Lee

Yoon lab's overall research motivation is to develop new therapeutic strategies to treat metabolic diseases. Traditionally, personalized medicine uses genetic characteristics and biomarkers of a disease to develop metabolic disease treatments, as in the case of cancer. Through my research, we suggest metabolite and nutrition can be used as the basis for the development of new treatments for metabolic diseases.
The Yoon laboratory focuses on the molecular regulation of cellular metabolism in metabolic disease using biochemical, cellular, and mouse modeling experiments approach. Cellular metabolism is altered by stress sensors. Cellular stress-sensors help maintains cell homeostasis. When cellular stress-sensing enzymes or the downstream effectors are dysfunctional, metabolism is rewired and alters cellular metabolic state. Especially, the mitochondrial enzymes of metabolism are tightly regulated by stress-sensing enzymes. Our goal is to investigate what proteins are capable of sensing cellular stress, how are they altered in metabolic disease. Since nutrient deprivation and oxygen deprivation are common stressors that a cell feels, our work focuses on cellular sensors that are responded to oxygen, and nutrient.

세포 에너지 대사 실험실에서는, 스트레스 감지 효소들이 mitochondrial fuel utilization, bioenergetic와 signaling에 미치는 영향을 생화학적 접근 방법으로 세포 및 마우스 모델 등을 이용하여 연구합니다. 신체에서 cellular 스트레스가 발생했을 때, 대사에 관여하는 metabolic enzyme은 stress-sensing enzymes에 의해 조절됩니다. 이런 metabolic 스트레스를 감지하는 효소 또는 하위유전자가 기능 이상일 때, 세포 대사 상태가 변화됩니다. 연구 목적은, metabolic enzyme이 신진 대사 질환에서 어떻게 변화하는지, 그리고 이러한 대사 결정 포인트가 정상적인 생리 및 대사 질환에서 표적연구가 가능한지 입니다. 특히, 영양소 부족과 산소 부족은 세포가 느끼는 일반적인 스트레스 요인이기 때문에, 저희 실험실에서는 산소와 영양소에 반응하는 대사 센서를 연구합니다.

Mebendazole preferentially inhibits cilia formation and exerts anticancer activity by synergistically augmenting DNA damage

Mitochondrial sirtuins: Energy dynamics and cancer metabolism

Metabolic Adaptation and Cellular Stress Response As Targets for Cancer Therapy

Lactate oxidase/vSIRPα conjugates efficiently consume tumor-produced lactates and locally produce tumor-necrotic H2O2 to suppress tumor growth

Gamma-Aminobutyric Acid Signaling in Damage Response, Metabolism, and Disease

FALCON systematically interrogates free fatty acid biology and identifies a novel mediator of lipotoxicity

Intrinsic myocardial defects underlie an Rbfox-deficient zebrafish model of hypoplastic left heart syndrome

Lipid metabolism in sickness and in health: emerging regulators of lipotoxicity

Extracellular vesicle proteomes shed light on the evolutionary, interactive, and functional divergence of their biogenesis mechanisms

SIRT4 is an early regulator of branched-chain amino acid catabolism that promotes adipogenesis

Development of a colorimetric a-ketoglutarate detection assay for prolyl hydroxylase domain (PHD) proteins

Obesity Shapes Metabolism in the Tumor Microenvironment to Suppress Anti-Tumor Immunity

PHD3 loss promotes exercise capacity and fat oxidation in skeletal muscle

Localized metabolomic gradients in patient-derived xenograft models of glioblastoma

Small-molecule screen identifies de novo nucleotide synthesis as a vulnerability of cells lacking SIRT3

FIH is an oxygen sensor in ovarian cancer for G9a/GLP-driven epigenetic regulation of metastasis-related genes

Metabolic recycling of ammonia via glutamate dehydrogenase supports breast cancer biomass

mTOR and HDAC inhibitors converge on the TXNIP/thioredoxin pathway to cause catastrophic oxidative stress and regression of RAS-driven tumors

PHD3 loss enables reliance on fat oxidation via deactivation of acetyl-CoA carboxylase

Distinct effects of SIRT1 in cancer and stromal cells on tumor promotion

Sirtuin 1 attenuates nasal polypogenesis by suppressing epithelial-to-mesenchymal transition

NAA10 controls osteoblast differentiation and bone formation as a feedback regulator of Runx2

Arrest defective 1 regulates the oxidative stress response in human cells and mice by acetylating methionine sulfoxide reductase A

Plant homeodomain finger protein 2 promotes bone formation by demethylating and activating Runx2 for osteoblast differentiation

Differential roles of Sirt1 in HIF-1α and HIF-2α mediated hypoxic responses

CITED2 controls the hypoxic signaling by snatching p300 from the two distinct activation domains of HIF-1α

Antihepatoma activity of chaetocin due to deregulated splicing of hypoxia-inducible factor 1α pre-mRNA in mice and in vitro

Obesity shapes metabolism in the tumor microenvironment to suppress anti-tumor immunity

Lipid metabolism in sickness and in health: Emerging regulators of lipotoxicity

PHD3 loss in cancer enables metabolic reliance on fatty acid oxidation via deactivation of ACC2

Antihepatoma activity of chaetocin due to deregulated splicing of hypoxia‐inducible factor 1α pre‐mRNA in mice and in vitro

Cellular Energy Metabolism Lab

교수님 소개

윤혜진

연구실 소개

연구실 키워드

알럼나이가 간 회사

연구실 지원 방법

대우 조건

연도별 논문 인용수

저널 & 학회 논문 출판 수

연구실 논문 목록

Mebendazole preferentially inhibits cilia formation and exerts anticancer activity by synergistically augmenting DNA damage

Mitochondrial sirtuins: Energy dynamics and cancer metabolism

Metabolic Adaptation and Cellular Stress Response As Targets for Cancer Therapy

연구실 보유 특허

대학별 입시끈

우리 연구실 모집

교수님 소개

윤혜진

연구실 키워드

알럼나이가 간 회사

연구실 지원 방법

대우 조건

연도별 논문 인용수

저널 & 학회 논문 출판 수

연구실 논문 목록

Mebendazole preferentially inhibits cilia formation and exerts anticancer activity by synergistically augmenting DNA damage

Mitochondrial sirtuins: Energy dynamics and cancer metabolism

Metabolic Adaptation and Cellular Stress Response As Targets for Cancer Therapy

연구실 보유 특허

최근 3년간 연구실적 높은 연구실

대학별 입시끈

우리 연구실 모집