My training brings me a strong background in basic science with a biochemical and molecular biological approach to my investigations. I am well versed in many gene expression systems such as transgenic exogenous expression of protein and CRISPR. I have performed radio-labeled binding, Western blot, ELISA, and PCR techniques in the cloning and evaluation of many protein targets. I have used bacterial expression, immunoprecipitation with and without chemical crosslinking, proximity-labeling of molecular partners, and yeast-2-hybrid to evaluate protein-protein interactions. I have also employed mouse model systems to investigate disease pathologies and several in vitro and in vivo imaging techniques. For a few specific examples, I have identified key determinants of protein amino acid sequence in the inositol 1,4,5-trisphosphate intracellular calcium release channel including the peptide sequences lining the channel pore. I have explored the genomic sequence preferences of the PiggyBac transposase enzyme and means by which it could be used to safely integrate transgenes into the human genome. I have performed investigations on T-cell mediated and mesenchymal stem cell therapies while working in the Texas Children’s current good manufacturing practices facility (cGMP). I have identified mitochondrial dysfunction as a key determinant of diabetic nephropathy progression. I demonstrated that phosphorylation of a specific serine in the mitochondrial fission factor, DRP1 is critical in diabetic kidney damage both in vitro and in vivo. I implicated that a long non-coding RNA, Tug1, plays an equally critical role in diabetic nephropathy by regulating both mitochondrial dynamic factors and transcriptionally modulating subunits of the electron transport chain. I have employed CRISPR knockout of pre-determined targets in T-cells to generate cells with greater resistance to inhibition in a tumor microenvironment. Recently, I have been involved in evaluating the role of cholesterol metabolism in diffuse large B-cell lymphoma (DLBCL) pathology. I have identified potential therapeutic targets in the signal transduction pathway regulation of cholesterol biosynthesis as key to DLBCL pathogenesis. Additionally, I have created a working mouse model to T-cell prolymphocytic leukemia in the immunodeficient NSG mouse. We have employed this mouse model to evaluate a combination drug therapy targeting the CDK and BCL2 pathways. My application of this background has been applied to translational research in the fields of biochemistry, physiology, immunotherapy, and nephrology.