Exposure to environmental pollutants and living in unhealthy environments contribute to a wide range of adverse health outcomes in our community, leading national recognition. The primary objective of the Environmental Disease Research Center is to conduct reasearch on the pathogenesis mechanism by which environmental factors cause or influence human diease and development for innovative methods for early detection, prevention, and control of environmentally-related diseases. The proposed center focuses on studying analysis of essential biomarkers of diseases induced by environmental pollutants and establishing validation or control system of various environmental disease. In particular, we are promoted to study for developing of novel targets and therapeutic candidates specific for particulate matters-mediated cell.
Research Areas
Establishment of a genome research infrastructure and technology platforms for environmental disease
Assessment of Ecotoxicological Effects of Particulate Matter in Human Organs
Development of particulate matter-induced pulmonary disease in mouse model and validation of novel therapeutic targets
Pathogenesis of environmental-related disease
Investigation of particulate matter(PM10/2.5)-mediated multiorgan failure
Development of stem cell models for environmental disease
Metabolic control and control of infectious disease using the macrophage, which is involved in innate immunity
Research on the mechanism of controlling metabolism by macrophage
Identification of mechanism for deterring infectious diseases and signaling control by macrophage
Study on environmental microbe(microbial toxin)-host interaction
Research on the mechanism of phagocytosis/efferocytosis
Development of immune cell for clearance damaged/senescent cells
Studies on the molecular mechanisms of particulate matter in cellular aging and aging-related diseases
Finding out the regulatory mechanism of necroptosis factor by ubiquitination
Finding out the mechanism of phagocytosis in bacterial infection
Selected Publications
Beclin 1 functions as a negative modulator of MLKL oligomerisation by integrating into the necrosome complex.
Cell Death Differ. 2020 Nov 27(9):3065
Jinho Seo (Co-first)
Exosomes released from Shiga toxin 2a-treated human macrophages modulate inflammatory responses and induce cell death in toxin receptor expressing human cells.
Cell Microbiol. 2020 Nov;22(11):e13249.
Moo-Seung Lee (Co-Corresponding)
Bacterial type III effector protein HopQ inhibits melanoma motility through autophagic degradation of vimentin.
Cell Death Dis. 2020 Apr 14;11(4):231
Young-Jun Park (Co-Corresponding)
Bioaccumulation of polystyrene nanoplastics and their effect on the toxicity of Au ions in zebrafish embryos.
