Daniel J. Prantner, PhD

University of Wisconsin- Madison, B.S., Biology

University of Arkansas for Medical Sciences, Ph.D., Microbiology and Immunology

Immunology has been a long-standing interest of mine dating back to coursework taken and benchwork performed as an undergraduate at the University of Wisconsin, Madison. Later, I specifically applied to microbiology and immunology programs because of their relevance to human health and my prior undergraduate classroom and research experiences in this field.

Subsequently, my doctoral training at the University of Arkansas for Medical Sciences under the tutelage of Dr. Uma Nagarajan and Dr. Roger Rank provided me with a more intensive focus on cellular microbiology and innate signaling pathways through advanced coursework and hands-on experiences.

In August 2010, I was fortunate to be selected to join the laboratory of my mentor, Dr. Stefanie Vogel, originally as a postdoctoral fellow, where I could gain intensive training in signal transduction pathways and understanding the biochemical basis of innate immune signaling. My introduction to this area led me to conceive and write a successful F32 grant application, that funded a project involving the regulation of signaling pathways by host mitochondrial metabolism, providing a wealth of knowledge about cellular metabolism. My most recent R21 grant involved the characterization of the metabolite methylglyoxal in a mouse model of sepsis.

Macrophages, Innate Immunology, Toll-like Receptors, Signal Transduction, Interferons, Sepsis

Prantner D, Vogel SN, Intracellular methylglyoxal accumulation in classically activated mouse macrophages is mediated by HIF-1α, J Leukoc Biol. 2024, qiae215, doi: 10.1093/jleuko/qiae215

Prantner D, Nallar S, Richard K, Spiegel D, Collins KD, Vogel SN. Classically activated mouse macrophages produce methylglyoxal that induces a TLR4- and RAGE-independent proinflammatory response. J Leukoc Biol. 2020. 109(3): 605-19.

Prantner D, Perkins DJ and Vogel SN.  2017. AMP-activated Kinase (AMPK) Promotes Innate Immunity and Antiviral Defense through Modulation of Stimulator of Interferon Genes (STING) Signaling. J Biol Chem. 2017.  292(1): 292-304.