I study two proteins, PAS-Kinase and USF1, and their roles in metabolic diseases. As we learn more about their mechanisms, interacting partners, and how to manipulate them we will be able to develop treatments and therapies for diabetes, obesity, and hyperlipidemia.
I am studying how the human systemic lupus erythematosus (SLE) IRF5 risk phenotype affects primary B cell activation and homeostasis. Collaborating with other researchers, I am investigating how SLE contributes to cancer and depression risk in lupus patients. By utilizing molecular and bioinformatic approaches, I hope to better understand environmental and genetic risk factors that contribute to systemic lupus erythematosus disease development.
My research focuses on uncovering the pathogenesis mechanisms of Chikungunya virus (CHIKV). CHIKV is a mosquito borne alphavirus which causes chronic arthritis. In the Robison lab we are interested in understanding how CHIKV evades the immune system and how this leads to chronic arthritis.
Helper T cells are activated when their T cell receptor (TCR) recognizes its specific peptide. I research how TCR-peptide affinity influences T cell proliferation and specificity through a panel of high affinity TCRs. I also investigate CD5—a coreceptor— role in T cell activation. This work has application for vaccine and immunotherapy development.
I study DNA replication in plant organelles. Compared to nuclei, their interactions and mechanisms are most likely much simpler, but this has yet to be well studied. Using bacterial and yeast cloning in conjunction with next generation sequencing, we hope to soon illustrate the interactions of plant organelle DNA replication proteins and their mechanisms.
I am interested in how bacterial pathogens evolve and adapt to survive in different conditions. I study what genes mammary pathogenic Escherichia coli needs to survive in the harsh environment of the mammary gland. I have employed genome-wide transposon insertion site sequencing to identify putative virulence factors needed to survive in diverse conditions.
Kai Li Ong
My research focuses on AMPK-oxysterol binding protein signaling pathway in controlling apoptosis, mitochondria morphology, and functions using yeast as a model organism. This would help in identifying a new drug target in treating metabolic diseases and cancer.
Antonio Solis Leal
I study a therapy to fight AIDS. To do so, I'm introducing a gene in Hematopoietic Stem Cells, which are the ones that produce CD4 T cells. This gene codes for a nuclease that specifically disrupts the HIV promoter. Thus, when an organism is exposed to HIV, there will be a resistant CD4 T cell population and the organism will be resistant to develop AIDS.
I work with bacteriophages, viruses that infect bacteria. I isolate and characterize novel bacteriophages that infect Erwinia amylovora, a bacteria that is known to cause a devastating disease called fire blight in fruit trees of rosaceae family.
I study T helper cells, important in adaptive immunity, with different CD5 expression. CD5 regulates T cell response. I am interested in the role that CD5 has upon activation by evaluating Ca2+ mobilization and metabolic response. I also study the molecular basis of immune dysfunction in nBMP2 mutant mice that suggest to have a defect in intracellular Ca2+ mobilization, important in immune response.
My research focuses on studying T cells. One project focuses on studying how altered peptides affect helper T cell activation in response to L. monocytogenes, a common food-borne pathogen. My other project focuses on developing antibodies that specifically target a novel cancer cell surface marker. This research can be applied to vaccine and immunotherapeutic design.
I work developing new cell adoptive therapies for cancer immunotherapy and doing tumor target discovery. My work consists of genetically engineering human immune system cells with tumor targeting receptors to selectively eliminate tumor cells.
Non Pictured Students
- David Bates
- Michelle Townsend