We have completed RAGE dimerization/oligomerization studies and a manuscript has been published. We continue to collaborate with colleagues in Australia to study RAGE thiol-disulfide bond exchange on the cell surface. Proteomics data showed that RAGE is acetylated. We are working with Johns Hopkins colleagues to study how such modification impact RAGE signaling and/or biology. We have recently deciphered the AGE-induced NF-kappaB RelA barcode, or signal-specific post-translational modifications, and linked the barcode to collagen I transcriptions in various cell types. Increased collagen content is a hallmark for aging-associated structural and functional changes in the vasculature. Our work, for the first time, established a direct link between AGE-RAGE axis and vascular aging phenotype. We are also actively studying the mechanism of RAGE shedding and trafficking in the cell, as well as spatiotemporal role of RAGE in signaling.
Peng, Yunqian; Kim, Ji-Min; Park, Hal-Sol et al. (2016) AGE-RAGE signal generates a specific NF-?B RelA ""barcode"" that directs collagen I expression. Sci Rep 6:18822 |
Low, Daren; Subramaniam, Renuka; Lin, Li et al. (2015) Chitinase 3-like 1 induces survival and proliferation of intestinal epithelial cells during chronic inflammation and colitis-associated cancer by regulating S100A9. Oncotarget 6:36535-50 |
Wei, Wen; Lampe, Leonie; Park, Sungha et al. (2012) Disulfide bonds within the C2 domain of RAGE play key roles in its dimerization and biogenesis. PLoS One 7:e50736 |