Labs
Lishko Lab
Couch Biomedical Research Building (MS: 8228-0041-01)
314-362-3566
lishko@wustl.edu
The focus of Lishko lab is on dissecting the role of bioelectricity in reproduction, aging, and metabolism. We are developing and applying advanced biophysical, biochemical, and cell biology methods to study how mammalian tissues and cells are regulated by unconventional steroid signaling and play a role in mammalian reproduction and neuronal functions. Specifically, our team studies the role of steroid-modulated ion channels in age-related macular degeneration, neurodegeneration, ovarian aging, and fertility. We also work on developing small-molecule-based therapies to treat reproductive and age-related disorders.
Nichols Lab
BJC Institute of Health (MS: 8228-0004-09)
314-362-6629
cnichols@wustl.edu
Research in my laboratory is focused on the biology of ion channels. We develop, introduce and use a wide range of molecular biological and biophysical approaches, as well as in vivo gene manipulation to address questions in proteins, cells and animals, and now in humans. These efforts are leading us to detailed understanding of both molecular mechanisms of channel activity, and roles of ion channels in multiple disease processes including diabetes, heart failure, pulmonary disease and epilepsy.
Pagliarini Lab
Couch Biomedical Research Building (MS: 8228-0041-01)
314-273-2330
pagliarini@wustl.edu
Mitochondrial Metabolism | Protein Biochemistry | Chemical Biology | Systems Genetics | Rare Diseases
Mitochondria are complex and dynamic organelles that are home to a vast array of essential metabolic pathways and processes and whose dysfunction underlies hundreds of human diseases. Despite this, much of the basic biology of these organelles remains obscure, and therapeutic options to treat mitochondrial dysfunction remain woefully inadequate. By blending classic biochemistry, molecular & cellular biology, and genetics with large-scale proteomics and systems approaches, our lab aims to systematically define the functions of uncharacterized mitochondrial proteins, identify new gene mutations that underlie human disease, and explore new molecular therapeutics to rectify mitochondria-based disorders.
Piston Lab
South Building (MS: 8228-0003-04)
314-747-8501
piston@wustl.edu
Fluorescence | Imaging | Quantitative Biology | Mathematical Models
Our lab focuses on understanding glucose-regulated hormone secretion from the islet of Langerhans, which is made up of glucagon secreting α-cells, insulin-secreting β-cells, and somatostatin-secreting δ-cells. Recent work has uncovered glucagon’s critical role in glucose homeostasis and the pathology of diabetes. Multiple signaling pathways arising from intrinsic glucose sensing, paracrine interactions and juxtacrine contacts within the islet all play a role in α-cell function. Our lab develops quantitative fluorescence technology broadly applicable to cell, tissue, and whole-organism imaging experiments. We apply these methods to assay living islet function quantitatively both ex vivo and in vivo, and these studies are proving critical to advancing our understanding of the regulation of glucagon secretion from α-cells.
Stewart Lab
BJC Institute of Health (MS: 8228-0004-07)
314-362-7449
sheila.stewart@wustl.edu
Senescence | Cancer | Immunotherapy | Therapy-induced Comorbidities | Age-related Cancer Drivers
Age remains the largest risk factor for the development of cancer, begging the question, what about aging drives the rapid increase in cancer we see in the 5th to 6th decade of life? While the answer is complicated, the Stewart laboratory focuses on how age-related changes in the tumor microenvironment contribute to tumor progression. This work includes delving into the mechanisms that drive senescence and secretion of pro-tumorigenic senescence associated secretory phenotype (SASP) factors. In addition, given senescent stromal cells recapitulate the phenotypes of cancer associated fibroblasts (CAFs), the laboratory also studies these important cells in both the primary and metastatic setting.
Stratman Lab
McDonnell Sciences Building (MS: 8228-0012-04)
314-273-7927
a.stratman@wustl.edu
Vascular Development | Cardiovascular Disease | Mechanobiology | Biophysical Regulation of Transcript/Gene Expression | Zebrafish | Live Time-Lapse Imaging | CRISPR Mutagenesis | Cell Signaling | Tissue Patterning | In Vitro Modeling
The Stratman lab studies signaling pathways regulating vascular development using zebrafish as a model system. Our ongoing research aims to understand how biomechanical forces, such as changes in tissue microenvironment or blood flow state, affect vascular patterning, signaling, and stabilization. Current lab projects focus on 1) the role of vascular primary cilia as mechanosensors, 2) the role of mechanical sensitive ion channels in regulating vascular stabilization, and 3) the role of endocytic trafficking and EVs in communication between the vasculature and the microenvironment.
True Lab
McDonnell Sciences Building (MS: 8228-0012-04)
314-362-3669
heather.true@wustl.edu
Protein folding and misfolding | Prions | Chaperones | Amyloid | Cellular Proteostasis | Degenerative neuromuscular disease mechanism
The True Lab is interested in the biological consequences of yeast prions - in both their capacity to function as novel epigenetic elements, as well as in their utility in modeling mechanisms of protein misfolding and aggregation that mimic important events in several neurodegenerative disorders. Additionally, we are interested in how prions in yeast impact survival and adaptation. We are also interested in understanding what other prions exist and how broadly prions affect cellular physiology. We are also using yeast prions to understand how the environment influences protein misfolding and aggregation, a question that has been difficult to address with current model systems of neurodegenerative disorders.
You Lab
McDonnell Sciences Building (MS: 8228-0012-05)
314-362-4668
zyou@wustl.edu
Replication Stress Response | DNA Damage Response | Nonsense-mediated RNA Decay (NMD)
We study molecular mechanisms that maintain genomic stability, focusing on DNA damage and replication stress responses and their relations to cancer formation and treatment. We also develop research tools for the NMD RNA surveillance pathway and investigate its intersection with genome maintenance pathways and its potential as a therapeutic target for specific hematological malignancies.