Oxidative stress

Cellular signaling in response to deleterious effects of oxidative stress - mainly we concentrate on the NRF2/KEAP1 and NF-κB molecular pathways and their role in signal transduction in response to oxidative stress-inducing agents: toxins, ionizing radiation, nanoparticles. In particular, we are interested in the mechanisms of expression of genes that are crucial in NRF2/KEAP1 and NF-κB signaling. These studies involve various molecular biology and biochemistry methods, among which Real-Time PCR, molecular cloning, temporary transfection, dual luciferase reporter system, gene fusions, Western blotting, imunocytochemistry and imunoprecipitation are most often used in CERAD. To answer the scientifically interesting questions, we perform our experiments on well established cellular models related to socially important maladies. We have studied NF-κB pathway in the cellular superoxide dismutase knockout mouse model in which cells are exposed to persistent oxidative stress in conditions that are related to oncogenesis and amyotrophic lateral sclerosis. Recently, we have started another project that will be realized using the cellular model of Parkinson’s disease. This project is focused on the role of PGAM5 protein in the relation between NRF2/KEAP1 and the programmed cell death pathways.