Research in the Shin Lab

The long-term research goal of the Shin lab is to understand the cellular roles of nuclear envelope proteins in development, metabolism and tumorigenesis. The lab aims to translate the acquired knowledge into developing therapeutic approaches for various human diseases linked to nuclear envelope protein dysfunction. To accomplish this goal, the lab has been using a variety of techniques including cell biology with advanced microscopy, biochemistry, mouse genetics, stem cell biology and multi-omics approaches.

One of the research directions is to delineate the roles of a nuclear envelope protein complex in hepatic steatosis and tumorigenesis. In a collaborative effort, the group discovered that the nuclear envelope localized LAP1-torsinA complex is responsible for hepatic lipid homeostasis whose abnormality is linked to steatotic liver diseases including steatohepatitis development (Shin et al. JCI, 2019). The current research focus is to investigate the underlying cellular and molecular mechanisms using mouse models in which LAP1 or torsinA is depleted from hepatocytes and isolated primary hepatocytes. A more recent research project funded by an NIH/NCI R01 grant is to investigate the novel mechanisms that can link alteration in the nuclear envelope to predisposition to hepatocellular carcinoma development in the setting of steatotic liver disease.

The lab is studying Emery-Dreifuss muscular dystrophy (EDMD) and related muscular dystrophies caused by mutations in genes encoding nuclear envelope proteins. Cardiomyopathies are a major life-threatening factor among these patients. The Shin lab is conducting multidisciplinary work in collaboration with an engineering group to establish preclinical human models to study the disease mechanisms of EDMD and associated cardiomyopathies.