Laboratories

Neurotransmission | Neurometabolism | Glycolysis | Mitochondrial Function | Synaptic Imaging | Neurodegeneration | Epilepsy

The overarching goal of the Ashrafi lab is to interrogate the metabolic regulation of synaptic transmission. We combine state-of-the-art imaging of single synapses with proteomic and genomic analysis to determine how metabolic pathways are regulated in the nervous system. We also investigate the dysregulation of mitochondrial and glycolytic energy metabolism in a variety of neurological disorders such as Parkinson’s disease and epilepsy.

Tumor Cell Signaling | Metabolomics | Proteomics | Transcriptomics | CRISPR screens | Molecular and Whole-Animal Imaging | Single-Molecule Biophysics | Targeted Therapy Development | Synthetic Organic Chemistry

The Blumer lab studies oncogenic signaling by mutationally activated heterotrimeric G proteins. Our ongoing research: 1) determines how oncogenic G proteins drive tumor formation, growth, invasion, survival, and metabolism; 2) establishes oncogenic G proteins as pharmacological targets for cancer therapy; and 3) designs and synthesizes G protein inhibitors for preclinical studies and, eventually, clinical trials. Much of our work focuses on metastatic uveal (ocular) melanoma because it is highly aggressive, deadly and untreatable, and nearly always driven by oncogenic G proteins.

Circular RNA (circRNA) | RNA Binding Protein (RBP) | RNA Structures | Hypoxia | Single-Cell RNA Sequencing (scRNA-seq) | RNA Therapy

The Chen lab utilizes multi-omic and high-throughput screening approaches to investigate the regulation and function of circRNA and uncover the molecular mechanisms of circRNA mediated disease. We aim to uncover (i) the RNA elements, genomic features, and protein components regulating the functions of circRNAs, (ii) the molecular mechanism of how circRNAs regulate cell physiology, and (iii) how circRNA dysregulation can lead to disease pathogenesis. Our long-term goal is to harness the unique properties of circRNAs to develop new tools for RNA-based technologies and therapeutic interventions.

Extracellular Vesicles | Exosomes | Adipose Tissue | Obesity | Diabetes | Metabolism

The Crewe lab uses transgenic mouse lines, cell culture and biochemistry to understand extracellular vesicle (EV)-mediated signaling during homeostatic and pathologic metabolic regulation. Our work has uncovered the existence of an expansive EV-mediated signaling network within the adipose tissue proper, and from the adipose tissue to other organs. This mostly adipocyte-derived EV population consists of exosome-like vesicles that carry proteins, RNAs and lipid species that can modulate a variety of signaling pathways in recipient cells. The focus of the lab is to determine how the various cargo of adipocyte EVs signal within the adipose tissue and from the adipose tissue to distal organs to modulate metabolism in obesity.

mRNA | MicroRNAs | Ribosomes | Translation | Gene expression | Neurodegeneration | Cancer

The Djuranovic Lab is primarily interested in understanding the mechanisms of post-transcriptional gene regulation. We focus on RNA-binding proteins (RBPs), ribonucleoprotein (RNP complexes) as well as mRNA sequence motifs, all of which control translational efficiency of their target mRNAs or are involved in general RNA metabolism.

Mass Spectrometry | Proteomics | Bioinformatics

We develop software, algorithms, and workflows for mass spectrometry and proteomics experiments. Using machine learning, statistical modeling, and computer science techniques we optimize a mass spectrometer’s data acquisition strategy in real-time to improve identification, quantification, and create novel analytical capabilities. We are focused on protein-protein interactions, protein complexes, and de novo peptide sequencing.

Tumor Microenvironment | Stress | Metastasis | Tumor Growth | Treatment Resistance | Metastatic Colonization | Tissue Microenvironment

The He Laboratory is utilizing it’s discovery of stress-induced NETs and novel mouse models, aiming to better comprehend the effects of systemic chronic stress on the CRC microenvironment. Specifically, we study the interplay between NETs, the immune populations, neuron and microbiota in mouse models of colitis and CRC.

Glutamate Receptors | Electrophysiology | Stem Cell Differentiation

We use electrophysiology to analyze neuronal synaptic function with a major emphasis on native and recombinant mammalian glutamate receptors. Our goal is to identify and characterize subtype-selective antagonists and allosteric modulators that enable dissection of the functional role played by specific receptor isoforms. We also study the differentiation of mouse and human embryonic stem cell and induced pluripotent stem cells into neurons in vitro, with a focus on assessing their terminally differentiated physiological characteristics.

Actin Cytoskeleton | Single Molecule TIRF Microscopy | Intracellular Trafficking | Cell Migration and Adhesion | Bone Mineralization

The Jansen lab addresses this question by studying how actin filaments are assembled and remodeled by posttranslational modification of actin monomers themselves as well as by the extensive family of actin-binding proteins, including Coronins, Plastins and Tropomyosins. Each of these protein families contribute to a wide range of diseases, including cancer, immunodeficiency, cardiovascular disorders, spinal muscular atrophy, and neurological defects, emphasizing their wide impact on cellular homeostasis and function through regulation of the actin cytoskeleton. To connect the molecular mechanisms with the cellular and pathophysiological roles of these actin-binding proteins, we are using a multipronged approach encompassing single molecule and microfluidics-assisted multi-wavelength TIRF microscopy, biochemical and biophysical assays, genetics, advanced co-culture systems, optogenetics and live-cell imaging. 

Imaging | Structural Biology | Metabolism | Organelle Contacts | Trafficking | Cytoskeleton

The Kast lab is investigating how cells remodel their metabolism in response to nutritional and environmental challenges. We are specifically interested in understanding the mechanisms cells employ to regulate the spatial-temporal arrangements and activities of metabolic compartments, such as lipid droplets, autophagosomes, and mitochondria, to meet the transient energy demands of the cell; as well as how perturbing these organelle networks contributes to pathogenesis of metabolic diseases and cancer. To study these processes, we use a multi-level approach that combines mass-spectrometry-based proteomics, cutting-edge microscopy, structural biology, and in vitro reconstitution assays.

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.

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.

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.

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.

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.

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.

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.

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.