Emily Fogarty, Phd Email & Phone Number

Tucson, Az, Us

United States

Golden, Co, Us

- Rapidly acquired knowledge of phosphoproteomic-based assay and its differentiators from competitors to educate prospective clients on applications of the technology- Developed and delivered customized scientific content to diverse audiences including scientists and clinicians to drive company growth- Designed and managed client projects to address their oncology program goals - Analyzed large scale proteomic data in Python and R to deliver data to clients and develop internal research protocols- Crafted accurate and compelling corporate communications to the public/media

Chicago, Il, Us

My graduate work in the Meren Lab combines metagenomic analyses of large datasets to generate hypotheses that I then test in the wet lab. Specifically, I co-led one project to develop a machine learning algorithm to predict naturally occurring plasmids in the human gut. I also led a project that combined genomics, metagenomics, genetic engineering, in vitro, and in vivo experiments to identify and characterize a particular plasmid that is prevalent across human populations and is constrained in its evolution. This near ubiquitous plasmid has the potential to act as a multifunctional biomarker for predicting inflammatory bowel disease and detecting human fecal contamination in water.

New Lambton, Nsw, Au

I was responsible for developing a project to examine the contribution of cellular senescence to idiopathic pulmonary fibrosis. This project was cell-culture based, and I developed and optimized the co-culture model of human lung fibroblasts with alveolar epithelial cells. I confirmed fibroblast senescence using ELISAs and Western Blots in both primary and immortalized cell lines, then tested the effects of these senescent cells on neighboring epithelial cells. I presented the work from this project in a talk at an international conference.

Vancouver, British Columbia, Ca

This project examined the effect of antibiotics on asthma development in a mouse model. Asthma is caused by dysregulation of the Type 2 immune system, and early life exposure to antibiotics is correlated with increased risk of asthma development in humans. I showed that early life administration of antibiotics to mice upregulates the levels of Type 2 cytokines responsible for B-cell class switching in the mesenteric lymph nodes, and that these mice have elevated levels of Type 2 antibodies (IgG1 and IgE) thought to be responsible for asthma development.

Thousand Oaks, Ca, Us

At Amgen, I was part of the biochemical screening group for therapeutic antibody development. I would process thousands of samples daily to identify antibodies binding to soluble targets, then characterize the strength of their binding interactions.

Doctor Of Philosophy - Phd, Microbiology

Bachelor Of Science - Bs, Microbiology And Immunology