구성원

구성원

김진기

Kim Jooyeon 김주연 교수

  • DepartmentDepartmentProf. Department of Medicine and Life Sciences, University of Science and Technology Convergence / Professor
  • E-mailE-mailjuyounkim@hanyang.ac.kr
  • Office PhoneOffice Phone031-400-5517
  • 학과/직책학과/직책과학기술융합대학 의약생명과학과 / 교수
  • 이메일이메일juyounkim@hanyang.ac.kr
  • 전화번호전화번호031-400-5517
Research Keywords
연구키워드
  • #Metabolism #Metabolic diseases #Therapeutics
  • #대사 병리 연구실
Research Objectives
연구목표
  • Our laboratory aims on identifying key molecular pathways regulating lipid, glucose and amino acid metabolism to treat metabolic disorders.
  • 대사의 불균형으로 인해 진행되는 만성 대사 질환의 원인규명과 치료를 목적으로 함.
Brief Research Experience
주요경력
  • 2000, Hanyang University, Bachelor in Biology
  • 2003, Yonsei University, Master in Biochemistry
  • 2012, Boston University, Ph.D. in Biochemistry
  • 2013-2017, University of California San Diego, School of Medicine, Post-doctoral research
  • 2018-2020, University of California San Diego, School of Medicine, Assistant project scientist
  • 2021-2022, University of California San Diego, School of Medicine, Staff research associate
  • 2023-Present, Hanyang University-ERICA, Department of molecular and life science, Associate Professor
  • 2000, 한양대학교, 이학학사
  • 2003, 연세대학교, 이학석사
  • 2012, 보스톤대학교, 의과대학, 이학박사
  • 2013-2017, 캘리포니아 샌디에고, 의과대학, 박사후과정
  • 2018-2020, 캘리포니아 샌디에고, 의과대학, 전임강사
  • 2021-2022, 캘리포니아 샌디에고, 의과대학, 전문 연구원
  • 2023-현재, 한양대학교, 과학기술대학, 부교수
Research Areas
연구분야
  • A) Study pathogenic metabolic alterations underlying non-alcoholic steatohepatitis (NASH) and other metabolic diseases.
  • B) Study lipid mediated cell fate decision
  • C) Identify therapeutic approaches for patients with metabolic disorders
  • A) 만성대사질환 (당뇨, 비 알코올성 간질환 등)에 관련된 병리학적 기전 연구
  • B) 지질에 의한 세포 운명 결정의 원리 연구
  • C) 대사 불균형으로 인한 난치성 대사질환을 치료하기 위한 유전자 치료와 세포 치료에 대한 연구
Thesis
논문
  • 1. Ju Youn Kim, Lily Q. Wang, Valentina C. Sladky, Tae Gyu Oh, Junlai Liu, Kaitlyn Trinh, Felix Eichin, Michael Downes, Mojgan Hosseini, Etienne D. Jacotot, Ronald M. Evans, Andreas Villunger, Michael Karin. PIDDosome-SCAP cross-talk controls fructose diet-dependent transition from simple steatosis to steatohepatitis.Cell Metabolism(2022), Oct; 34:1548-1560.*Co-responding Author
  • 2. Elodie Bosc, Julie Anastasie, Feryel Soualmia, Pascale Coric,Ju Youn Kim,Lily Q.Wang,Gullen Lacin, Kaitao Zhao, Ronak Patel, Eric Duplus, Philippe Tixador, Andrew Sproul, Bernard Brugg, Michelle Reboud-Ravaux, Michael Shelanski, Serge Bouaziz, Michael Karin, Chahrazade El Amri, and Etienne Jacotot.Genuine Selective Caspase-2 Inhibitionwith new Irreversible Small Peptidomimetics.Cell Death and Disease(2022), Nov; 13:1~14.
  • 3. Ju Youn Kim, Feng He, Michael Karin. From Liver Fat to Cancer:Perils of the Western Diet.Cancers(2021),Mar;13 (5): 1-19.Hsiao-Yen Ma, Jun Xu, Gen Yamamoto, Sara B. Rosenthal, Ludmil B. Alexandrov, Daniel Karin,Ju Youn Kim, Sven Heinz, Chris Benner, Yukinori Koyama, Takahiro Nishio, Shuang Liang, Mengxi Sun, Xiao Liu, Gabriel Karin, Peng Zhao, Pnina Brodt, Iain H. Mckillop,OswaldQuehenberger, Ed Dennis, Alan Saltiel, Hidekatzu Tsukamoto, Bin Gao, Michael Karin, David A. Brenner, Tatiana Kisseleva. IL-17 signaling in steatotic hepatocytes and macrophage promotes alcohol-induced HCC.J. Hepatology(2020) May;72: 946-959.
  • 4. Ju Youn Kim, Ricard Garcia-Carbonell, Shinichiro Yamachika, Peng Zhao, Debanjan Dhar, Rohit Loomba, Randal J. Kaufman, Alan R Saltiel, Michael Karin. ER Stress Drives Lipogenesis and Steatohepatitis via Caspase-2 Activation of S1P.Cell(2018) Sept;175: 1-13.
  • 5. Ricard Garcia-Carbonell, Jerry Wong,Ju Youn Kim, Lisa Abernathy Close, Brigid S. Boland, Thomas L Wong, Philip A Harris, Samuel B Ho, Soumita Das, Peter B Ernst, Roman Sasik, William J Sandborn, John Bertin, Pete J Gough, John T Chang, Michelle Kelliher, David Boone, Monica Guma and Michael Karin. ElevatedA20 promotes TNF-induced and RIPK1-dependent intestinal epithelial cell death.Proc Natl Acad Sci USA.(2018) Sept;12:1-9.
  • 6. Debanjan Dhar, Laura Antonucci, Hayato Nakagawa,Ju Youn Kim, Elisabeth Glitzner, Stefano Caruso, Shabnam Shalapour, Ling Yang, Mark A Valasek, Sooyeon Lee, Kerstin Minnich, Ekihiro Seki, Jan Tuckermann, Maria Sibilia, Jessica Zucman-Rossi, Michael Karin. Liver Cancer Initiation Requires p53 Inhibition by CD44-Enhanced Growth Factor Signaling.Cancer Cell(2018) Jun;33(6):1061-1077
  • 7. Laura Antonucci, Johan B. Fagman,Ju Youn Kim, Jelena Todoric, Ilya Gukovsky, Mason Mackey, Mark H. Ellisman, Michael Karin. Basal autophagy maintains pancreatic acinar cell homeostasis and protein synthesis and prevents ER stress.Proc Natl Acad Sci USA. (2015) Oct;28:1-9.
Research Topics
연구내용
The major interests of our lab are to investigate the role of lipid in development of metabolic diseases. Specific research focus are on 1) how lipids regulates hepatocyte fate, 2) how lipids metabolism regulates the development of non-alcoholic fatty liver disease (NAFLD), 3) to identify the molecular pathway underlying NASH development.

Triglyceride and cholesterol are important metabolites, regulating diverse pathways, of which dysfunctions are closely associated with liver disease incidence and progression. Triglyceride functions as energy storage, and protects hepatocytes from damage and genetic mutation while cholesterol is the major component of lipid raft, a small invagination of the plasmamembrane, thatfunctions as molecular carrier and the hurb of a signal transduction. However, how these lipidsleadto the development of NAFLD remains unclear. Non-alcoholic steatohepatitis (NASH) is a metabolic disorder, account for 30% of incurable liver disease and defined as inflammation-associated fatty liver, which potentiates the liver aggravation to deadly liver failures, cirrhosis and hepatocellular carcinoma. In our laboratory, we use diet-induced NASH mouse models, established by using transgenic mice inwhich particularlipid pathway is impaired. Along with NASH mouse models, we incorporate the advanced research techniques, including but not limited to metabolomics, lipidomics, single cell analysis, proteomics as well as wet-lab biochemistry. With the mouse models mimicking the human NASH pathology and advantages from advanced techniques, we will understand metabolic pathways underpinning NASH development in depth and aim on identifying the target molecules applicable to therapeutic approaches for the patients with NASH.