I direct a robust research program focused on dissecting the molecular mechanisms that control adaptive responses to metabolic stress and pro-inflammatory signals in adipose tissue, immune cells and breast cancer. To achieve this goal, we use a combination of basic molecular biology and biochemical approaches (site-specific mutagenesis, CRISPR editing, gene expression analyses, protein-protein interaction studies, in vitro enzymatic assays), next generation sequencing (ChIPseq, RNAseq, GROseq) and in vivo studies (tissue-specific mouse models, dietary challenges, cold exposure, tumor xenografts). Since 2017 I also serve as co-Director of the BNORC Adipose Biology and Nutrient Metabolism Core which provide access to mouse and human adipocytes/pre-adipocytes and banked tissues, and consultation/training for applications related to adipose tissue biology, obesity and nutrition to BNORC members in the broad Boston area.
References
1. Cardamone MD, et.al. A protective strategy against hyperinflammatory responses requiring the non-transcriptional actions of GPS2. Molecular Cell, 2012;46:91-104.
2. Huang J, et.al. Exchange Factor TBL1 and Arginine Methyltransferase PRMT6 Cooperate in Protecting GPS2 from Proteasomal Degradation. JBC 2015; 290:19044-54.
3. Cederquist C.T., et.al. Systemic insulin sensitivity is regulated by GPS2 through inhibition of AKT ubiquitination and activation in the adipose tissue. Molecular Metabolism, 2016;6:125- 137.
4. 4. Lentucci C., et.al. Inhibition of Ubc13-mediated ubiquitination by GPS2 regulates multiple stages of B cell development. JBC, 2017;292:2754-2772.
Last Updated on September 29, 2020