Research at the Laboratory of Inflammatory Genes focuses on the signals and mechanisms that are critical to the expression regulation of inflammatory genes and their functional role in the immune responses. In addition, we are also interested in understanding the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in the unfolded protein response (UPR) that is triggered by endoplasmic reticulum (ER) stress. Regarding innate immune response, we have found unanticipated new role for the antiviral protein kinase PKR in protozoan parasitic infection both in vitro and in vivo. Yet, a gene that is under current investigation in the lab encodes a Toll-like receptor (TLR)-inducible Ras guanine exchange factor member 1b (RasGEF1b). Using the state-of-art Cre/LoxP strategy, we have generated a number of tissue conditional knockout mice to investigate the effects of RasGEF1b deficiency in inflammatory responses both in vitro and in vivo. Thus, we established the first mouse model for the study of tissue-specific deletion of Rasgef1b and we are describing, for the first time, the role of RasGEF1b in macrophages and in vivo.
Therefore, knowing how the proteins encoded by the inflammatory genes work we will certainly improve our understanding to develop novel therapeutics to combat infectious and inflammatory diseases and prevent tissue damage.
Regarding studies on NSAIDs, we have found the transcription factor ATF6 in the ER stress pathway as a novel molecular target for the biological actions of aspirin metabolite sodium salicylate.
With these studies under progress, my lab fosters critical thinking about mechanisms regulating the TLR-mediated innate immune and ER stress responses in a setting where dissemination of ideas to a diverse audience is valued.