The general focus of our group is on the transcriptional and epigenomic control of inflammation, and especially on the molecular mechanisms of the anti-inflammatory actions of glucocorticoids (GC) – steroid compounds that remain the most commonly prescribed class of drugs for a majority of inflammatory and autoimmune diseases. Despite their clinical efficacy, GC are prone to causing serious side effects, especially on the bone and metabolism. The design of more specific 'new generation’ GC-like medications requires a better understanding of how conventional GC function. We have been studying the transcriptional cofactors of the GC receptor (GR) and, more broadly, inflammation-relevant transcription regulators that control gene expression programs in macrophages – a central cell type to mediate protective as well as pathogenic inflammatory pathways. We rely on molecular biology, biochemistry and genomics to understand the transcriptional and chromatin networks that govern macrophage identity and gene expression, we engineer mouse strains lacking key components of suspect pathways and evaluate these mice in animal models of disease. By doing so, we have been able to identify novel critical players that regulate inflammation in vitro and in vivo that can be tested in future translational studies that will help understand mechanisms of disease pathogenesis in humans and ultimately improve patient care.
We are looking for POST-BAC fellow!! Please contact us if interested.
CONGRATS TO SANDA AND TEAM FOR NEUROINFLAMMATION PAPER https://bit.ly/3diroo4
R01 (NIH/NIAID) - Post-initiation control of transcription in inflammatory macrophages (DEC 2019)
R01 (NIH/NIDDK) - Glucocorticoid-regulated transcription networks in macrophage biology (JULY 2019)
R21 (NIH/NINDS) - The role of transcriptional cofactor GRIP1 in microglia-driven neuroinflammation (ARPIL 2019)
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