Amy Hauck

Assistant Professor
Biochemistry, Molecular Biology, and Biophysics

Signal-dependent, rhythmic transcription of metabolic pathways is essential for maintaining physiological homeostasis, and the disruption of these signaling networks is a strong driver of metabolic disease. Our research is focused on how metabolic signals are integrated within the nucleus by a family of transcription factors called nuclear receptors (NRs) and their coregulators to coordinate gene expression patterns, with an emphasis on how derangements in NR signaling and function contribute to metabolic disease.

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Research statement

Nuclear receptors (NRs) are potent, signal-dependent transcriptional regulators critical for maintaining metabolic flexibility at the cell, tissue, and systems levels. Disrupted NR activity is implicated in metabolic dysfunction and contributes to the prevalence and progression of diseases including metabolic dysfunction-associated steatotic liver disease (MASLD) and Type II Diabetes. We seek to interrogate the mechanisms that dictate and differentiate between distinct activities of NRs in tissue- and disease-specific conditions with the ultimate goal of being able to better modulate NR function to combat metabolic disease.

In the Hauck lab, we use an integrated multi-omic approach and novel mouse models to explore the signals and coregulators that determine NR function and genomic occupancy and to identify the enzymatic mechanisms upon which they rely for signal-dependent chromatin remodeling and transcriptional regulation.

Education and background

Postdoctoral Fellow - University of Pennsylvania, Institute for Diabetes, Obesity, and Metabolism

PhD in Biochemistry (BMBB) - University of Minnesota, 2017

BA in Biology - University of San Diego (2010)