MSCSLMetabolic Syndrome and Cell Signaling Laboratory

Research

Our work starts from insulin signaling and extends to muscle, mitochondria and cancer metabolism.

  • Insulin signaling and metabolic syndrome

    Our interest lies in the molecular mechanisms of insulin signaling. Insulin is the primary anabolic hormone of the body and stimulates glucose uptake into muscle, liver and fat. Loss of insulin production, or deregulated insulin signaling in tissues such as liver, leads to type 1 and type 2 diabetes.

    We focus on a family of proteins at key points of the PI3K/PKB (AKT) pathway. PKB/Akt couples activation of the insulin receptor to glucose uptake, cell growth, cell survival, angiogenesis and gene regulation. Our own work concerns new members of this pathway, namely PHF20, CTMP and LETM1.

  • Muscle and mitochondria

    We study how the PHF20–YY1 axis regulates PGC-1α, TFAM and COX IV, which drive mitochondrial biogenesis and function in skeletal muscle, and how failure of this axis contributes to sarcopenia. Muscle-specific PHF20 knockout mice are one of our main tools.

  • Targeted protein degradation

    We use targeted protein degradation (TPD) to look for drug candidates against sarcopenia. This work is linked to the development program of Mitos Therapeutics Inc., a biomedical venture founded by Prof. Park in 2020.

  • Cancer energy metabolism and drug resistance

    Cancer cells rewire their energy metabolism, and mitochondria have been a theme of our work since Prof. Park's sabbatical at the University of Cincinnati. Current projects address anticancer drug resistance in ovarian cancer and temozolomide resistance in glioblastoma, including the roles of cathepsin A (CTSA), CD14 and lysosomal biology.