Last updated Sat, Jan 4 2024
This page is currently being updated to more effectively represent everything that I’ve worked on over the years. Please bear with me while I finish it up!
Protein engineering at U. Chicago Molecular Engineering
As a postdoctoral scientist in the Mendoza Lab, I use display-based libraries to engineer cytokines and their receptors to manipulate their signaling properties with the ultimate goal of designing next generation protein therapeutics.
Structural immunology at U. Chicago Biology
As a graduate student in the Adams Lab I worked mainly on two proteins that play important roles in the innate and adaptive immune response: the archaic HLA-B*73:01 and the non-classical HLA-F. Both molecules serve as ligands for the germline-encoded, polymorphic Killer-immunoglobulin-like receptors (KIRs), but how this occurs and the consequences thereof were unclear when I began my work.
In the case of HLA-B*73:01, it was known that similar to other class I molecules, HLA-B*73:01 presents “short” peptides on the surface of cells. However, what I was interested was in what ways HLA-B*73:01 was different to other class I molecules. To learn more about HLA-B*73:01, check out our preprint here, while the manuscript is under review.
In the case of HLA-F, the questions were more fundamental. It was thought that unlike other class I molecules, HLA-F did not need to form a heterodimer with β2M in order to be expressed on the surface of cells. Charlie Dulberger, a former mentor of mine in the Adams lab, showed that HLA-F could also present peptides similar to all other class I molecules. So then which is the “true” form and what regulates the expression of these different forms? A preprint of my work on HLA-F is in preparation as well.
For the most thorough overview of my graduate work, feel free to check out my thesis.
Plasmodium computational genomics in the Llinás Lab
As a member of the Llinás Lab I contributed to work in understanding transcriptional regulation in the deadliest human-infecting parasite that causes malaria, Plasmodium falciparum.
Primary contributions resulted in the following publications:
- Red Blood Cell Invasion by the Malaria Parasite Is Coordinated by the PfAP2-I Transcription Factor
- Refining the transcriptome of the human malaria parasite Plasmodium falciparum using amplification-free RNA-seq
Want to investigate our data yourself? Use this Shiny App I developed for doing so!
You should also check out the generous commentary on our study here: Scientists on a RAMPAGE to find apicomplexan transcription start sites
Additional contributions resulted in the following publications: