Research

The Boron Lab studies how gases such as CO2, O2 and NH3 cross cell membranes. Contrary to long-standing dogma, we found that gases don't simply diffuse through membrane lipids—they require dedicated gas channels, such as aquaporin-1 (AQP1) and the Rh proteins, which can also select between different gases. We also study how cells regulate intracellular pH (pHi) and how gases cross biological membranes—two processes fundamental to nearly every aspect of cell function, from metabolism and division to signal transduction. Our discovery that cells actively regulate pH launched decades of work identifying the underlying molecular machinery, including the electrogenic Na+/HCO3− cotransporter NBCe1, the first Na+-coupled HCO3− transporter ever cloned. Together, these research areas aim to reveal how cells sense and manage their acid-base environment in health and disease.

Information coming soon

The Dai lab integrates biochemistry, cryo-EM structural biology and cell biology for hypothesis-driven, mechanistic studies aimed at uncovering the molecular logic underlying human diseases and identifying disease-modifying therapeutic targets. Our research spans a broad range of topics, with particular interest in viral infectious diseases, innate immunity, lytic cell death pathways and inflammatory diseases. Recent examples of our work in these areas include structural studies of human herpesvirus fusion proteins for vaccine design (Science Advances, 2026; PMID: 42497258), structural mechanisms of SAMD9 autoinhibition and pathogenic dysregulation in MIRAGE syndrome (Science Advances, 2026; in press), and the structural basis of NINJ1-mediated plasma membrane rupture in lytic cell death (Cell, 2025; PMID: 39667936).

The Decker Aerospace Lab investigates how the human brain and body respond to extreme and operationally demanding environments. Our research spans neuroimaging, high-altitude physiology, and sleep and fatigue science, with a focus on oxygen stress, cognitive vulnerability, and the limits of human performance in aerospace and high-risk settings. The Decker Aerospace Lab is dedicated to advancing the understanding of human physiology in extreme and operational environments, with a particular focus on aerospace and applied human performance. Our work integrates principles of physiology, engineering, and translational research to investigate how the human body responds to stressors such as hypoxia, altitude, acceleration, and altered oxygen delivery. By combining laboratory-based experimentation with real-world applications, we aim to generate insights that improve safety, performance, and resilience in aviation and other high-demand settings.

Visit the Decker Aerospace Lab.

Areas of Concentration: 

• Ion channel physiology
• Subcellular organelle physiology
• Cellular mechanisms of inflammation and innate immunity
• Regulated cell death physiology

The Dubyak Lab studies how cells sense tissue damage and microbial invasion to regulate inflammatory and innate immune responses in health and disease. These biological stresses often induce the release of ATP and other nucleotides from intact or damaged cells. The released nucleotides stimulate P2 receptors on nearby cells to rapidly induce adaptive responses such as vasodilation, hemostasis and inflammation.

Released nucleotides belong to the group of so-called DAMPs (Danger-Associated Molecular Patterns), which include other normally intracellular molecules that, when released into extracellular compartments, entrain innate immune and inflammatory responses. A common theme of the lab research is the interaction between DAMPs and inflammasome signaling.

The Dubyak Lab also studies several proinflammatory signaling responses triggered by extracellular ATP and other DAMPs in murine and human leukocyte models, including:

• Post-transcriptional and ionic signals that regulate assembly of inflammasome signaling platforms
• Inflammasome-mediated pathways for non-classical secretion of IL-1beta and other inflammatory mediators
• Mechanisms for extracellular accumulation of ATP and other DAMPs in inflammation and cancer
• Regulated cell death signaling pathways during inflammation

Innate Immune Activation and Podocyte Injury in Diabetic Kidney Disease

The Gonzalez-Vicente Lab studies how metabolic stress in diabetes activates innate immune pathways and drives proinflammatory cytokine production in glomerular cells. The lab integrates data from diabetic animal models with multi-omics datasets from patients with diabetic kidney disease (DKD). The goal is to identify molecular subtypes that explain part of the heterogeneity in DKD pathogenesis and to define patient populations that may benefit from targeted therapies.

Pathogenesis of APOL1-Associated Kidney Diseases

Genetic variants in the APOL1 gene, which are enriched in populations of African ancestry, are associated with an increased risk of chronic kidney disease. The pathogenic mechanisms underlying this genetic association remain incompletely understood, and the lack of consensus regarding how APOL1 risk variants induce kidney disease has hindered the development of targeted therapies.

Research in the lab focuses on glomerular and single-cell transcriptomes from human kidney tissue and organ models to identify transcriptional phenotypes associated with APOL1 kidney risk variants. The goal is to identify gene signatures that inform the pathobiology of APOL1-associated nephropathies and help identify potential therapeutic targets.

Team Science

The Gonzalez-Vicente Lab emphasizes team science and collaborates with kidney investigators and NIH consortia, particularly the Nephrotic Syndrome Study Network (NEPTUNE) and the Kidney Precision Medicine Project (KPMP). The lab also contributes to WikiPathways as community editors with a focus on renal genomics.

Areas of Concentration:

• Computational modeling of oxygen delivery and hemoglobin-oxygen affinity (P50)
• Red blood cell gas transport physiology (O 2 , CO 2 )
• Aquaporins, Rhesus proteins, and non-canonical gas-channel transporters
• Acid-base physiology and Na+-coupled bicarbonate transport
• Quantitative fluorescence methods (FRET, imaging flow cytometry) and systems-level/transcriptomic analysis

Dr. Moss investigates the molecular and biophysical mechanisms governing how solutes and gases cross cell membranes, with long-standing expertise in acid-base homeostasis and oxygen transport in red blood cells (RBCs). His multidisciplinary collaborations with Dr. Walter F. Boron and colleagues have contributed to our ongoing understanding of how cells regulate their intracellular pH in response to changes in their local environment, and of how transmembrane gas permeability is largely mediated by protein channels, rather than by passive diffusion through the lipid bilayer. Building on this foundation, Dr. Moss is developing an independent computational research program translating membrane biophysics into clinically actionable measures of tissue oxygen delivery. Dr. Moss’s research employs quantitative fluorescence imaging and systems-level analysis — including single-cell transcriptomic profiling of hippocampal neuron-astrocyte cultures — to characterize cellular heterogeneity underlying acid-base regulation. He extends this same expertise to collaborative projects beyond RBC and acid-base physiology, including immunofluorescence studies that complement single-cell transcriptomic and STING-pathway studies of kidney disease with Dr. Agustin Gonzalez-Vicente, quantitative fluorescence approaches to membrane protein interactions in metabolic disease models with Dr. Jeffrey Schelling’s laboratory, and primary neuronal culture and cell-biology support for structural studies of synaptic kainate receptor complexes with Dr. Nami Tajima’s laboratory.

Areas of Concentration: 

• Understanding the molecular mechanisms underlying ion channel folding, assembly and degradation
• Ameliorating ion channel misfolding diseases

Proteostasis Maintenance of Membrane Proteins in Health and Disease

The Mu Lab studies protein homeostasis (proteostasis) of ion channels, which are major drug targets involved in numerous neurological, neurodegenerative and cardiovascular diseases. 

To function, ion channel proteins must fold into their native structures and assemble properly in the endoplasmic reticulum (ER) for subsequent trafficking to the plasma membrane in a fully functional state. Variations in a given protein can lead to protein misfolding and excessive degradation through the ER-associated degradation (ERAD) pathway or autophagy, resulting in reduced concentrations of proteins in cell membranes and loss of function.

Current research in the lab focuses on neurotransmitter receptors, including gamma-aminobutyric acid type A (GABAA) receptors, the primary inhibitory ion channels, and N-methyl-D-aspartate (NMDA) receptors, the major excitatory ion channels in the human brain. These receptors mediate the inhibition-excitation balance in the mammalian central nervous system, and their dysfunction is associated with epilepsies, autism and other neurodevelopmental diseases.

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Areas of Research Concentration

• G protein–coupled receptor (GPCR) signaling regulation in health and disease
• Cardiovascular Hemodynamics
• Renal physiology and chronic kidney disease mechanisms
• Hormonal, neurotransmitter, and mechanosensory signaling pathways
• Hypertension and blood pressure regulation
• Pregnancy-related cardiovascular and renal complications
• Translational signaling research and therapeutic target discovery
• Integrative physiology and whole-body functional analysis
• Pharmacological modulation of GPCR signaling
• Genetically engineered animal models of human disease

The Osei-Owusu Lab in the Department of Physiology and Biophysics investigates how cell signaling pathways are integrated and regulated to control cardiovascular and renal function in health and disease. The lab focuses on signaling mediated by heterotrimeric G proteins, which are primarily activated by G protein–coupled receptors (GPCRs) and tightly regulated by GTPase-activating proteins such as RGS
proteins. Because dysregulated GPCR signaling contributes to a wide range of human disorders—including hypertension, heart failure, chronic kidney disease, diabetes, stroke, and depression—and because more than half of all therapeutic drugs target GPCRs, this work is central to understanding normal physiology and disease mechanisms while identifying new opportunities for therapeutic intervention.

Using approaches rooted in pharmacology and integrative physiology, the Osei-Owusu Lab studies signaling across multiple levels of biological organization, from molecules and cells to tissues, organs, and genetically engineered animal models that recapitulate human disease. In collaboration with other investigators, the lab pursues translational research projects focused on pregnancy-related complications,
hypertension, chronic kidney disease, and spinal cord injury. By emphasizing whole-body function and clinically relevant models, the lab aims to advance fundamental knowledge of GPCR signaling and contribute to the development and optimization of treatments for cardiovascular and renal diseases.

The Osei-Owusu Lab in the Department of Physiology and Biophysics investigates how cell signaling pathways are integrated and regulated to control cardiovascular and renal function in health and disease. The lab focuses on signaling mediated by heterotrimeric G proteins, which are primarily activated by G protein–coupled receptors (GPCRs) and tightly regulated by GTPase-activating proteins such as RGS
proteins. Because dysregulated GPCR signaling contributes to a wide range of human disorders—including hypertension, heart failure, chronic kidney disease, diabetes, stroke, and depression—and because more than half of all therapeutic drugs target GPCRs, this work is central to understanding normal physiology and disease mechanisms while identifying new opportunities for therapeutic intervention.

Using approaches rooted in pharmacology and integrative physiology, the Osei-Owusu Lab studies signaling across multiple levels of biological organization, from molecules and cells to tissues, organs, and genetically engineered animal models that recapitulate human disease. In collaboration with other investigators, the lab pursues translational research projects focused on pregnancy-related complications,
hypertension, chronic kidney disease, and spinal cord injury. By emphasizing whole-body function and clinically relevant models, the lab aims to advance fundamental knowledge of GPCR signaling and contribute to the development and optimization of treatments for cardiovascular and renal diseases.

Areas of Concentration: 

• Mitochondrial biology and pathology
• Metabolism
• Neuron-immune interaction
• Neurodegenerative diseases
• Drug discovery

Mitochondrial Quality Control and Neurodegenerative Disease

The Qi laboratory investigates how mitochondrial quality control and metabolism contribute to neurodegenerative diseases. Research in the lab focuses on key mitochondrial pathways, including mitochondrial dynamics, proteostasis, genome maintenance, and communication between mitochondria and other organelles, to understand how mitochondrial dysfunction disrupts cellular homeostasis and promotes neuronal vulnerability.

Using proteomics, genomics, cellular and molecular biology, patient iPSC-derived models and disease animal models, the laboratory identifies disease-relevant mitochondrial mechanisms and explores therapeutic strategies to target them. This work includes the development of rationally designed peptide inhibitors, modulators of protein-protein interactions and high-throughput screening approaches, with the long-term goal of advancing mitochondrial medicine for neurodegenerative diseases.

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Areas of Concentration: 

• Neurodegenerative Diseases
• Cancer
• Cardiovascular Disease

Molecular Biophysics of Mitochondrial Dynamics and Synaptic Vesicle Endocytosis

Cellular membranes undergo dynamic changes in shape in remarkably striking ways during processes such as cell movement and division, and also during vesicle fission and fusion events that are integral to intracellular membrane trafficking. Large, mechanochemical GTPases of the dynamin superfamily are critically involved in many of these events including those of synaptic vesicle recycling, clathrin-mediated endocytosis, mitochondrial division and fusion, and peroxisome biogenesis. They often work in concert with membrane-sculpting BAR domain-containing proteins and various accessory molecules in effecting membrane fission and fusion. The main objective of our research is to reconstitute and elucidate the various molecular machineries and mechanisms involved in intracellular membrane remodeling, fusion and fission, specifically in synaptic vesicle endocytosis and mitochondrial dynamics, using cutting-edge state-of-the-art fluorescence spectroscopic techniques, including FRET, FCS, FLIM and related biophysical methodologies.

FATP2 and Diabetic Kidney Disease

The Schelling laboratory utilizes molecular and cellular methods, animal models and human samples to investigate the pathophysiology of diabetic kidney disease (DKD). The lab made the initial discovery that proximal tubule cell apoptosis leads to tubular atrophy, which strongly predicts DKD progression.

Current research focuses on the roles of fatty acid transport protein-2 (FATP2) in proximal tubule lipotoxicity and the effects of FATP2 inhibition on plasma glucose reduction through pancreatic a-cell-mediated GLP-1 secretion and paracrine stimulation of b-cell insulin release.

The lab is also investigating the mechanisms of proximal tubule FATP2-mediated mitochondrial fission and endoplasmic reticulum lipid bilayer stress, as well as the development of FATP2 inhibitors as potential treatments for diabetes and DKD.

Areas of Concentration:

• Nervous system
• Cardiovascular system

Sympathetic Nervous System and Cardiovascular Function

The overall goal of the Smith laboratory is to understand the physiology of sympathetic nervous system activation in the regulation of the acute “fight or flight” sympatho-adrenal stress reflex and the sympathetic control of cardiovascular function.

Cardiac therapeutics and gene therapy applications for the treatment of various forms of heart disease

The Cardiovascular Therapeutics Laboratory, led by Julian Stelzer, focuses on the molecular mechanisms involved in cardiac muscle function and the functional roles of contractile proteins in heart disease. The pumping action of a healthy heart relies on the coordinated contraction and relaxation of cardiac muscle driven by the sarcomere. In heart disease, sarcomere function can be disrupted by genetic anomalies that cause structural changes, cell signaling disruptions and phosphorylation changes.

The lab studies the functional effects of post-translational modifications of contractile proteins at both the myofilament and in vivo whole-organ levels, as well as how genetic defects in these proteins lead to altered cross-bridge function and impaired contractile function.

Research in the lab utilizes a variety of molecular and biophysical techniques to study cardiac muscle mechanics, including knockout and transgenic animal models, in vivo gene transfer techniques, echocardiography, pressure-volume catheterization and magnetic resonance imaging.

Visit the Stelzer Lab.

Our group utilizes biochemical and biophysical approaches to address questions of protein misfolding in neurodegenerative diseases, including prion diseases, Alzheimer’s disease, amyotrophic lateral sclerosis, and frontotemporal dementia. The current focus is largely on two projects:

The role of liquid-liquid phase separation (LLPS) in protein aggregation and neurodegenerative diseases. 

One of the most intriguing recent developments in cell and molecular biology are the findings regarding the critical role of protein liquid-liquid phase separation (or biomolecular condensation) in many biological and biochemical processes. However, increasing body of evidence indicates that there is also a darker side to this phenomenon. In particular, LLPS appears to be associated with the pathogenesis of some of the most devastating neurodegenerative disorders. Using biophysical, biochemical and cellular techniques, our lab is seeking to understand the mechanism of LLPS of proteins involved in these diseases and uncover the relationship between LLPS, protein aggregation and the pathogenic process. The proteins of particular interest in this regard are tau and TDP-43. Tau is a major player in Alzheimer's disease (AD) and several other disorders collectively known as tauopathies, whereas aggregation of TDP-43 is associated with amyotrophic lateral sclerosis and frontotemporal dementia (FTD).

High-resolution structural studies of prions and other amyloid fibrils.

Accumulation of amyloid-like fibrils in the nervous system is a common feature of many neurodegenerative diseases such AD, prion diseases, FTD and Parkinson’s disease. Recent findings indicate that fibrils formed by the same protein can exist in a multitude of structurally distinct forms, and that these structurally distinct amyloid "strains" may be responsible for phenotypic variability of not only prion diseases but also other neurodegenerative disorders. Our lab is using biophysical methods, including cryo-electron microscopy, to determine these structures and gain insight into the relationship between amyloid structural polymorphism and disease phenotype.

Visit the Surewicz Lab.

Area of Concentration:

• Cell autonomous and innate immunity
• Host-pathogen interaction
• In situ cryo-electron tomography

At the Zhu Lab, we investigate how mammalian cells detect and respond to intracellular pathogens—bacteria, viruses, fungi, and parasites—focusing on the molecular interface where host defense meets microbial adaptation. Our work is organized around three questions: how invading microbes are sensed, how that recognition is translated into immune signaling, and how pathogens are ultimately sterilized despite their defense mechanisms. We address these questions using a multidisciplinary approach centered on cryo-electron tomography (cryo-ET), complemented by cryo-EM, in vitro reconstitution, advanced imaging, and molecular and cell biology, allowing us to visualize immune complexes and infection events directly within their native cellular context. We are equally interested in the in situ high-resolution structure and function of macromolecular complexes driving bacterial pathogenesis, and we actively develop new cryo-EM/ET methods to push the throughput and resolution of in situ structural cell biology. Our goal is to uncover the molecular mechanisms of host defense and use that knowledge to inform new strategies against infectious disease.

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