서재명

Ph.D.

Star Library

Genetics, Development, Metabolism

  • 042-350-4247 (lab. 042-350-4269)
  • jmsuh@kaist.ac.kr
  • 대사비만당뇨 통합 연구실(iMOD)
LAB WEBSITE
  • 연구분야

    본 연구실의 연구 주제는 대사 현상의 조절과 관련되어 있는 과정을 이해하는 것이다. 우리는 다양한 접근 방법 으로 대사 현상을 연구하고 있으며 현재는 정상 상태와 병리학적 상태에서의 지방조직, 근육, 뇌와 외분비선에 관한 연구를 진행하고 있다. 연구를 진행하기 위해 주로 마우스 모델을 활용하고 있고 이와 더불어 세포생물학 및 분자생물학적 기법도 활용하고 있다.
    지방조직 리모델링과 대사질환의 연결고리가 되는 기전들을 밝히기 위한 다양한 실험적 접근을 통해 비만, 당뇨와 같은 현대병을 극복할 과학적 토대를 마련하고자 한다.

     

    Welcome to the integrated laboratory of Metabolism, Obesity, Diabetes (iMOD)–Suh laboratory! Our research focuses on understanding the processes that are involved in the regulation and execution of metabolism. While we are interested in understanding metabolism from a variety of angles, the lab currently focuses on adipose, muscle, brain and exocrine gland function in normal and pathological states. Our research primarily utilizes mouse models along with various cell and molecular biological tools to address questions in the following areas.

    • PPARgamma-FGF1 axis in adipose tissue remodeling and metabolic flexibility
    • PPARdelta-FGF1 axis in muscle regeneration and aging
    • Brain FGF signaling in nutrient and metabolic responses
    • Adipose secretome analysis by proximity ligation
    • Adipose tissue aging and senescence mechanisms
    • Mechanisms of Tph1 in adipose tissue thermogenesis
    • Mechanisms of ERRgamma in exocrine gland function
    • Discovery of novel pathways involved in CNS injury and repair
    • Adipose tissue dedifferentiation mediated by growth signaling pathways
    • Mechanisms of FGF mediated radiomitigation during intestinal injury

    We are seeking talented and motivated students and post-docs to join our research team and inquiries can be made by directly contacting Dr. Jae Myoung Suh at jmsuh@kaist.ac.kr

  • Major
    Publications
    • Kim, K.E., Park, I., Kim, J., Kang, M.G., Choi, W.G., Shin, H., Kim, J.S.#, Rhee, H.W.#, Suh, J.M.#. Dynamic tracking and identification of tissue-specific secretory proteins in the circulation of live mice. Nat Commun (2020)

      in revision (#co-corresponding author)

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    • Yeom, E., Shin, H., Yoo, W., Jun E., Kim, S., Hong, S.H., Kwon, D.W., Ryu, T.H., Suh, J.M.#, Kim, S.C.#, Lee, K.S.#, Yu, K.#. Tumor-Derived Dilp8/INSL3 induces cancer anorexia by regulating feeding neuropeptides via Lgr3/8 in the brain. Nature Cell Biology (2020)

      in press (#co-corresponding author)

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    • Suh, J.M.*,Jonker, J.W.*, Ahmadian, M.A., Goetz, R., Lackey, D., Huang, Z., Osborn, O., van Dijk, T., Yoshihara, E., Liu, W., Havinga, R., Fan, W., Yin, Y., Yu, R.T., Liddle, C., Atkins, A.R., Olefsky, J.M., Mohammadi, M., Downes, M., Evans, R.M. Endocrinization of FGF1 produces a neomorphic and potent insulin ensitizer. Nature (2014)

      513, 436-9. (*co-first author)

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  • 연구실 소개
    대사비만당뇨 통합 연구실(iMOD)