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My current work centers on the development of two murine models that will force expression of the opposing splice variants of CPEB2 (Cytoplasmic Polyadenylation Element Binding Protein). Past studies within Dr. Park’s lab have demonstrated that the alternative splicing of CPEB2 may be one of the mechanisms behind the regulation of HIF1a - a transcription factor highly expressed during hypoxia. The two isoforms, CPEB2A or CPEB2B, appear to impact HIF1a in opposing fashions. By exposing our murine models (one expressing isoform A, and one expressing isoform B) to decreased levels of O2, we will be able to study the role that these splice variants play in regulating HIF1a, and thus regulating the detrimental ailments that follow hypoxia: including pulmonary hypertension, leakage/edema, and tissue remodeling

I received my Honours Bachelor Of Science in the Specialist (Co-operative) Program in Molecular Biology & Biotechnology from the University of Toronto on June 2019. I had worked for 1 year as a lab assistant in Beijing Genomics Institution (BGI) where I acquired many practical biological and molecular biological techniques, including CRISPR/Cas9. After I joining the CMMB Master program at USF in the Fall of 2019, my current research focuses on the study of the G protein-coupled receptors (GPCR) to develop better therapies for GPCR-related neurodegenerative diseases and cancers.

I received my B.S. in Microbiology from Kansas State University in December 2014 before joining the CMMB Ph.D. program at USF in the Fall of 2015. My work centers on developing novel therapeutics targeting the ESKAPE pathogens, with a particular focus on the eradication of biofilms and persister cells.

Clear cell renal cancer (RCC) originates in the lining of small tubules in the kidney. Although there exist effective treatment regimens, mortality remains high when the disease metastasizes. RCC is a metabolic disease and is characterized by the presence of lipid droplets. However, the mechanisms underlying the lipid dysregulation in RCC remains unclear. My project will focus on elucidating the pathways (specifically the contribution of non-coding RNAs) that could lead to this metabolic abnormality.

Sinkholes are common features in Florida. However, little is known about the microbial communities within these sinkholes. I am investigating how the geochemistry influences the microbial community structure over time in a stratified anchialine sinkhole located in the Weeki Wachee River, which is known as Hospital Hole. I am also working with engineering to determine if the microbial communities from the anoxic zones of several sinkholes are able to degrade fish waste in an anaerobic microcosm digester to create methane, which may be used for energy.

Paramyxoviruses include notable pathogens such as Measles, Nipah, and Newcastle disease virus that infect both humans and animals. Paramyxoviruses use the concerted action of two membrane proteins to infect, a receptor binding protein (RBP) and a fusion (F) protein. Upon binding of the receptor, the RBP activates F to carry out fusion of the host and cell membranes. The receptor binding site and the f activating site on the RBP are separated by >2 nm. Moreover, experiments suggest that receptor binding induces negligible structural changes within the RBP monomers, suggesting that a change in dynamics may play a central role in signal transmission between the two sites. I use computational tools to understand the dynamic allostery that links the receptor binding and the F activating sites in the Newcastle RBP.

Cancer development is influenced by gene expression patterns via epigenetic mechanism (DNA methylation, chromatin packaging, and histone modification). Epigenetic modifiers are essential for directing lineage-specific transcriptional programs in immune cells. Disruption of these cellular processes contributes to the progression of various hematological malignancies. Small-molecular inhibitors against chromatin and histone modifiers have proven to be effective in the clinic. My work focuses on understanding the epigenetic processes responsible for the progression of T-cell and B-cell leukemia, and identifying key targetable mechanisms in these diseases. Special AT-rich sequence binding protein 1 (SATB1) is an essential epigenetic modifier for T-cell development in the thymus. Interestingly, we have found that SATB1 is either transcriptionally repressed or overexpressed in many leukemia/lymphomas of various lineages compared to normal lymphocytes. As such my research aims to: 1.) Understand the role of SATB1 in 3D chromatin modification/looping structures in conjunction with other chromatin-associated factors. 2.) Understand how the epigenetic silencing/overexpression of SATB1 expression in leukemia/lymphomas trigger molecular reprogramming and pathology. 3.) Screening epigenetic inhibitors and their efficacy in targeting oncogenic or restoring tumor suppressive pathways.

I earned a B.S. in Biomedical Sciences from the University of South Florida in the fall of 2016. During my undergraduate career, I worked in the Shaw lab alongside Rahmy Tawfik on the development of novel therapeutics from Actinobacteria. I joined the doctoral program in the spring of 2017, performing my dissertation research on novel antibacterial agents derived from marine sources.

I earned a B.S. in Cell and Molecular Biology and in Public Health from USF in Spring 2015. I then continued on to obtain an M.S. degree in Public Health with a concentration in Global Communicable Diseases from USF in Spring 2017. I am currently a Ph.D. student in the Shaw lab, and my research centers on novel pathways that regulate virulence determinant production in Staphylococcus aureus.

My current research focuses on the role that RNA alternative splicing plays in the progression of breast and lung cancer. About 1 in 8 women will develop breast cancer in her lifetime, and roughly 1 in 15 men or 1 in 17 women will develop lung cancer in his or her lifetime. Current drug therapies struggle to treat these common and high-mortality cancers due to their heterogeneous genomic and transcriptomic profiles, Hence, personalization of therapeutic regimens requires a multi-omics approach. Using deep RNA sequencing data, I aim to identify both alternative mRNA splicing and non-coding RNA pathways which play key roles in tumor development and metastasis through 3 projects: 1) The role of alternative mRNA splicing and non-coding RNA pathways in non-transformed breast cells compared to tumorigenic breast cancer cell lines, 2) The role of alternative mRNA splicing in non-coding RNA pathways in various lung cancer oncogenotypes including Kras and p53 mutants, and 3) The role of alternative mRNA splicing in non-coding RNA pathways in a murine breast cancer Cers4 knockout model.

I received my B.S. in agricultural biotechnology from the University of Kentucky in 2015. Upon graduating, I worked as a research analyst at ParaTechs Corporation on projects enhancing baculovirus expression systems and the use of modified viruses as control agents. After gaining admission to the CMMB doctoral program in Fall 2016, I joined the Shaw lab. My research centers on sRNA regulation in MRSA with a specific focus on virulence enhancing entities.

I received my B.S. in Conservation Biology from Kansas State University in 2016. At USF, I'm researching underwater caves and sinkholes with the goal of developing strategies for conserving these strange, wild ecosystems.