Through our genomic studies using human blood and atherosclerotic plaque tissue samples, we have identified a marker of atherosclerosis disease severity and a cholesterol-independent marker of statin treatment, which has been granted a use patent. We have also identified tristetraprolin zinc finger protein 36 (TTP) as a mediator of localized tissue inflammation important for inflammatory arthritis and atherosclerosis. With our interest in oxidative stress and metabolism which affect inflammation, a driver of atherosclerosis, we are pursuing studies to examine the effect of altered p53 signaling on the immune system using specific genetic models.
| Kang, Ju-Gyeong; Sung, Ho Joong; Amar, Marcelo J et al. (2016) Low ambient oxygen prevents atherosclerosis. J Mol Med (Berl) 94:277-86 |
| Zhuang, Jie; Ma, Wenzhe; Lago, Cory U et al. (2012) Metabolic regulation of oxygen and redox homeostasis by p53: lessons from evolutionary biology? Free Radic Biol Med 53:1279-85 |
| Kang, Ju-Gyeong; Amar, Marcelo J; Remaley, Alan T et al. (2011) Zinc finger protein tristetraprolin interacts with CCL3 mRNA and regulates tissue inflammation. J Immunol 187:2696-701 |
| Kang, Ju-Gyeong; Sung, Ho Joong; Jawed, Sarah I et al. (2010) FOS expression in blood as a LDL-independent marker of statin treatment. Atherosclerosis 212:567-70 |
| Biesecker, Leslie G; Mullikin, James C; Facio, Flavia M et al. (2009) The ClinSeq Project: piloting large-scale genome sequencing for research in genomic medicine. Genome Res 19:1665-74 |
