Dr. Bonini was awarded his PhD in Biochemistry and Molecular Biology in 2004 by the University of Sao Paulo, (Brazil). In 2004 he moved to start his postdoctoral training at the laboratory of Dr. Ronald P. Mason, at the National Institute of Environmental Health Sciences focused on the understanding of how redox driven reactions affect signaling events relevant for the maintenance of mitochondrial energetic function and carcinogenesis. In 2009, he established an independent, multidisciplinary program focused on the identification of redox sensitive pathways involved in tumor progression and metastasis at the University of Illinois at Chicago. At UIC he rose to the rank of Associate Professor and Director of the Redox Biology Program. In 2018 he joined the Medical College of Wisconsin as a Tenured Associate Professor of Medicine (endocrinology). His laboratory at MCW is interested in determining how changes to the electrochemical potential of the nucleus changes the chromatin epigenetic landscape, the interaction of transcription factors with co-regulators and genomic loci, and how these events regulate gene transcription involved in breast cancer progression and inflammatory diseases.
Biophysical Forces Regulating Gene Transcription in Cancer
This project is based on the hypothesis that variations in the redox state of the nucleus change the chromatin epigenetic landscape as well as the shape of transcriptional complexes leading to the recognition of alternative DNA loci and the expression of genetic programs enacting adaptation to stress or disease. We use tools to generate oxidants at specific cellular organelles (inclusive of the nucleus), to interrogate if redox changes in the nucleus serve as triggers of gene expression programs linked to diseases caused by environmental exposures or aging.
S-Nitrosation regulates macrophage polarization in response to inflammatory stimuli
This project is based on the observation that nitric oxide produced in the nucleus serves as a redox regulator of NF-kB activity and macrophage (pro-) or (anti-) inflammatory activation. Our studies showed that this different modality of oxidation (NOS1-driven S-nitrosation) of suppressor of cytokine signaling-1 (SOCS1) inhibits the activity of the enzyme as a negative regulator of inflammation. These studies indicate that the duration and intensity of redox signals originating from NOS1 in the nucleus define the course, locality and duration of inflammation.