Cells under ER stress employ signaling events called the “unfolded protein response” (UPR) to restore ER homeostasis. Among signaling molecules in UPR, X-box binding protein 1 (XBP1s) is one of key signaling molecules and has been shown to play a crucial role in the hypothalamus, liver and pancreatic β cells’ metabolic regulation. There is “cross-talk” between XBP1s and other signaling molecules including p38 MAPK, IKKβ, Brd7, PI3K and FoxO1. Furthermore, XBP1s interactome is critically involved in metabolic homeostasis. These findings clearly demonstrate that ER stress and its related signaling pathways are critically important in metabolic regulation.
Our research interests stem from the existence of various interactions surrounding UPR and their critical involvement in metabolic homeostasis, and their subsequent potentials as therapeutics toward obesity, type 2 diabetes and other metabolic disorders. We identify novel interactions between UPR and other signaling pathways and investigate their roles in metabolic homeostasis. Our research currently focuses on the following topics.
1. Identification of novel crosstalk between UPR and other signal transduction pathways (UPR interactome)
2. Identification of novel post-translational modifications (PTMs) on UPR signaling molecules (such as phosphorylation and ubiquitination)
3. Investigation of the physiological role of crosstalk and PTMs of UPR on energy, glucose and lipid metabolism
4. Investigation of the pathophysiological role of crosstalk and PTMs of UPR on the development of obesity, type 2 diabetes and other metabolic disorders.
Advisor Professor : Lee, Jae Min