| Faculty | Research interest/projects | |
|---|---|---|
| Gerry Apodaca, PhD | gla6@pitt.edu | Our lab studies epithelial cell biology and mechanotransduction. Lab rotation opportunities include the following: 1. Use confocal microscopy, scanning EM, and TEM to define the organization of the umbrella cell apical junctional complex (AJC) during filling and voiding of the bladder. 2. Use viral transduction of tagged-AJC components coupled with live-cell imaging to develop techniques to visualize AJC dynamics in the native urothelium. Ultimately, we will use these tools to define whether there are roles for membrane traffic (exocytosis and endocytosis), as well as the actin/intermediate cytoskeleton in these events. 3. Use conditional knockout mice to explore the function of mechanosensitive PIEZO channels in lower urinary tract function. More info: https://apodaca2.dept-med.pitt.edu |
| Michael Butterworth, PhD | michael7@pitt.edu | Our lab focuses on the role of microRNAs in (sex-specific) renal sodium handling and kidney disease. We use KO and gain-of- function mouse models with primary and engineered cell lines to investigate the hormonal regulation of microRNAs in the kidney. Findings are linked to in vivo models of kidney injury. More info: www.butterworthlab.com |
| Christopher Cunningham, PhD | cunningc@pitt.edu | The Cunningham Lab is interested in understanding the neural and sensory biology of the vertebrate auditory system. Many unique and highly specialized proteins with exquisitely precise subcellular localizations are critical for each step of sound processing. Hearing loss is the most common sensory deficit, and multiple forms of hearing loss involve aberrant proteostasis—improper assembly, trafficking, and/or regulation of key auditory proteins. We utilize mouse models of human deafness for our experiments. The similarities between the rodent and human auditory systems allow for a panoply of experimental manipulations that aim to uncover basic biological mechanisms and translational insights relevant for human health. The lab utilizes cutting-edge techniques including the generation and analysis of novel genetic mouse models combined with biochemistry, molecular biology, histology, viral vectors and high-resolution fluorescent microscopic imaging. Ultimately, we hope to utilize our findings toward the development of new therapies for hearing loss and deafness. To this end, we are very interested in developing gene therapy strategies that can treat hearing loss. More info: thecunninghamlab.com |
| Yiqin Du, MD, PhD | yiqindu@pitt.edu | Our current main projects are 1) exploring the feasibility and mechanisms of stem cells and their trophic factors for trabecular meshwork regeneration and extracellular matrix turnover for glaucoma treatment; 2) combining stem cells and bioengineering to treat corneal scarring and corneal endothelial dystrophy. We work on different types of adult stem cells and iPSCs. Please visit: https://ophthalmology.pitt.edu/research/research-laboratories/stem-cell-biology-glaucoma-laboratory |
| Partha Dutta, DVM, PhD | duttapa@pitt.edu | 1. Epigenetic regulation of inflammation in macrophages 2. Crosstalk of inflammatory cells and the central nervous system 3. Regulation of macrophage-mediated inflammation by cellular metabolism 4. The role of microglia in cognitive impairment in cardiovascular disease Please visit https://duttalab.pitt.edu/ |
| Zach Freyberg, MD, PhD | freyberg@pitt.edu | In Situ Cryo-Electron Microscopy Approaches to Investigation of Vesicle Trafficking Dopamine’s Role in Regulation of Insulin Release See more |
| Arjumand Ghazi, PhD | ghazia@pitt.edu | We study the biology of aging using a combination of molecular genetic and genomic approaches in the model system, C. elegans. In particular, we focus on genes that link lifespan to reproduction, reproductive aging and aspects of healthspan such as immunity. Current rotation projects will expand on our recent studies on: 1. Alternative splicing of endocannabinoid-producing genes during pathogen response and aging: This project focuses on our discovery that a pro-longevity protein, TCER-1 (homolog of human transcription elongation and splicing factor, TCERG1), represses immunity, depending on the status of the animal’s fertility (Amrit et al., Nature Communications, 2019). Using a combination of genomic and molecular-genetic analyses, we have found that TCER-1 represses immunity by regulating the alternative splicing of lipases responsible for endocannabinoid production. The rotation project will address the role of this alternative splicing event in healthspan. 2. Mechanisms by which germline dysfunction accelerates somatic aging: Our lab recently demonstrated that impairing germline health by disrupting meiosis reduced lifespan, accelerated loss of protein homeostasis and healthspan and triggered premature aging in C. elegans, through a potentially conserved molecular signature (Loose et al., Aging Cell, 2022). The rotation project will detail the decline in different aspects of somatic proteostasis in progeric meiosis mutants. 3. Maternal-embryonic fat transport during health, aging and disease. Using integrated genomic, lipidomic and molecular approaches, we have recently made exciting, unpublished discoveries on the mechanisms by which lipid transport from the mother to the embryo is controlled and its dysfunction during maternal infections. The rotation project will document the impact of age and on this process and the role of specific lipid species. Please visit: http://www.chp.edu/CHP/ghazilab |
| Gerry Hammond, PhD | ghammond@pitt.edu | We use single-cell chemi- and opto-genetics and synthetic biology to dissect lipid signaling in cancer and other diseases. Please visit: https://hammondlab.com/ |
| Yang Hong, PhD | yhong@pitt.edu | The lab focuses on the molecular mechanisms regulating cell polarity, using both Drosophila and cultured cells as model systems combined with cutting-edge live imaging approaches (https://elifesciences.org/articles/79582). In recent years our lab has made breakthrough discoveries that established electrostatic membrane targeting as a fundamental mechanism in regulating cell polarity. Our research has so far revealed that the electrostatic membrane targeting of polarity proteins can be regulated by various mechanisms such as phosphorylations, allosteric conformation changes, and coincident protein interactions. Moreover, we discovered a striking phenomenon that the electrostatic membrane targeting can be severely disrupted by acute and reversible depletion of membrane PI4P and PIP2 triggered by hypoxia and ATP inhibition, suggesting a novel mechanism underlying the disruption of cell polarity in the ischemia-reperfusion injury and tumorigenesis. Visit: http://www.cbmp.pitt.edu/people/faculty.html?id=1016 |
| Ossama Kashlan, PhD | obk2@pitt.edu | Our lab is interested in the molecular mechanisms of ion transporter regulation, including the epithelial Na+ channels (ENaC) and the sodium-hydrogen exchanger (NHE3). We are particularly interested in direct interactions with biological and pharmacological ligands. We use a variety of approaches that include functional, biochemical, physiological, and computational approaches. Our current projects are 1) determine the physiological effects of ENaC activation by bile acids in the context of liver disease using mouse models and patient samples, 2) determine the relationship between the structure of ENaC and its function using evolutionary and functional approaches, and 3) determine whether SGLT2 inhibitors exert their effects by inhibiting non-SGLT2 targets. See more |
| Thomas Kleyman, MD | kleyman@pitt.edu | The Kleyman lab has a longstanding interest in epithelial transport physiology, particularly with regard to how structure relates to function. The lab focuses on ion channels in the distal aspects of the nephron, including epithelial Na+ channels (ENaC), large conductance Ca2+ activated K+ channels (BK), and mechanosensitive Piezo channels. See more |
| Adam Kwiatkowski, PhD | adamkwi@pitt.edu | A long-term objective of the Kwiatkowski Lab is to gain a deep, mechanistic understanding of cardiomyocyte adhesion and cytoskeletal organization at the intercalated disc. Our approach is to define mechanisms of cell-cell adhesion, and downstream regulation of actin and intermediate filament organization, by the cadherin/catenin family of adhesion proteins. This is a significant biomedical problem because mutations in cell adhesion and cytoskeletal proteins at the intercalated disc are linked to cardiomyopathies. The Kwiatkowski Lab takes an interdisciplinary approach to biomedical research. We combine protein biochemistry, cell biology, proteomics, bioengineering, and light and electron microscopy to study cell adhesion at the molecular and cellular levels. Potential rotation projects using cultured primary cardiomyocytes and combining advanced live cell fluorescence microscopy with biochemistry include: 1) determining how ligand recruitment to the cadherin/catenin complex promotes cadherin organization and intercalated disc assembly; and 2) defining how external mechanical cues are sensed and transduced through adhesion complexes to regulate cardiomyocyte organization. For more information on the Kwiatkowski lab, see: www.kwiatkowskilab.com |
| Todd Lamitina, PhD | stl52@pitt.edu | Our lab uses the worm C. elegans for addressing questions in basic and translational sciences. There are 2 main projects in the lab. Project 1) Organismal responses to osmotic stress - regulation of cell volume is the most aggressively defended physiological setpoint in virtually every organism. But in multicellular animals we understand very little about how deviations in cell volume brought on by osmotic stress lead to changes in physiology and behavior. We use genetic screens and neurobiological approaches, two of the greatest strengths of the C. elegans system, to understand how this organism adapts to osmotically stressful environments. Project 2 ) Models of neurodegenerative disease - Neurodegenerative diseases, such as ALS, are devastating and currently incurable genetic diseases. Introducing ALS gene mutations into C. elegans causes worms to develop age-dependent paralysis via loss of motor neurons. We utilize unbiased genetic screening in these ALS models to identify the mechanisms of neurodegeneration, with an eye towards developing new therapeutic approaches. More details can be found on our website: https://toddlamitina.wixsite.com/lamitina-lab |
| Partha Roy, PhD | par19@pitt.edu | Our lab studies the role of actin cytoskeleton regulatory proteins and transcriptional factors in metastatic breast cancer, renal cancer, angiogenesis (physiological and pathological).and endothelial cell-immune cell crosstalk. We adopt a wide range of in vitro and in vivo experimental techniques, bioinformatics analyses, small molecule screening, and live cell imaging. For detailed information, please visit https://www.engineering.pitt.edu/subsites/faculty/roy/cell-migration-lab/ |
| Jami Saloman, PhD | jls354@pitt.edu | We use an interdisciplinary approach to investigate neural interactions with other cellular systems. We are interested in normal organ function, chronic pain, and tumorigenesis. Ongoing projects include 1) the role of neuronal PDL1 in cancer pain, 2) neuronal regulation of tumor growth and anti-tumor immunity, and 3) peripheral circuits controlling pancreas function and pancreatitis. Visit https://salomanlab.pitt.edu/ |
| Yusuke Sekine, PhD | SEKINEY@pitt.edu | Y. Sekine Lab is working on the molecular mechanisms and cellular stress responses that allow a cell to adapt to metabolic alterations, and their relevance to human aging and age-related diseases. Website: https://aging.pitt.edu/labs/sekine-y-lab/ |
| Shiori Sekine, PhD | sekine@pitt.edu | S. Sekine lab is working on precise molecular mechanisms by which mitochondria sense internal/external insults/environmental changes and trigger appropriate cellular responses. We aim to enhance human health based on basic biological research. Website: https://www.shiorilab.net |
| Sunder Sims-Lucas, PhD | sus58@pitt.edu | The Sims-Lucas laboratory focuses on therapeutics related to kidney injury. We use a combination of cell based models and mouse models of human kidney injury with a particular focus on the role that fatty acid oxidation plays in mediating kidney injury. More info: https://www.pediatrics.pitt.edu/divisions/nephrology/labs-and-faculty-pages/sims-lucas-lab |
| Alexander Sorkin, PhD | sorkin@pitt.edu | Project 1. Define temporarily resolved interaction networks of EGF receptor using proximity-labeling mass-spectrometry and characterize newly-discovered components of these networks. Project 2. Analyze localization dynamics of the active receptor tyrosine kinases in mouse tumors in vivo using cancer cells that are engineered to express a novel fluorescent sensor using CRISPR gene-editing. See more |
| Arohan Subramanya, MD | ars129@pitt.edu | Our lab explores the relationship between biomolecular condensates, signaling, and cellular and whole animal physiology. Biomolecular condensates are membraneless organelles that assemble via liquid and/or gel phase transitions. We study WNK kinases, a family of serine threonine kinases that regulate cell volume by activating within condensates in response to intracellular crowding. Kidney tubule cells use this process to control ion flux, blood pressure, and potassium homeostasis. Much of our work is centered around understanding how molecular crowding is sensed and controlled in cells, and how condensates influence salt and water balance in mammals. We use a combination of approaches including live cell imaging, gene editing of cells and mice, proteomic analysis of cells and kidney tissue, whole animal physiology, and condensate analysis in human patient samples. More here: http://www.subramanyalab.org/ |
| Stella Sun, PhD | stellasun@pitt.edu | Sun lab is working on the flagellar protein trafficking that is critical for cell motility and cell-cell communication in Trypanosoma brucei (T. brucei), a single celled-parasite which causes African sleeping sickness in humans and Nagano in cattle. By using molecular and cell biology, and the cutting-edge cryo-electron tomography (cryo-ET) with allied techniques such as cryo-FIB-SEM, we are dedicated to understanding the cellular structure and function of flagellum in cell migration and cell-cell communication. With the advanced imaging techniques, we can visualize the organization of cellular structures and their coordination in 3D spatial organization through a multi-scale imaging platform ranging from microns to sub-nanometers, to elucidate the molecular and structure functions that drive cell motility. More events please see our lab website: https://sunlab.structbio.pitt.edu/ |
| Jay Tan, PhD | jay.tan@pitt.edu | We study the cell biology of aging: (1) lysosomal quality control in health and disease (2) innate immunity in aging and age-related disease. JayTanLab.org |
| Michael Tsang, PhD | tsang@pitt.edu | We are interested in elucidating the molecular mechanism of heart regeneration. We employ genome editing to determine gene function and transcriptome profiling to identify critical factors in zebrafish heart regeneration. See more |
| Karina Vargas, PhD | kvargas@pitt.edu | We study synuclein physiological and pathological function in the synapse. We have several projects for rotation including the study of synuclein molecular interaction with different endocytic proteins and lipids in heath and disease. Visit https://synapsephysiologylab.com/ |
| Deepika Vasudevan, PhD | deepika.vasudevan@pitt.edu | The lab's research is aimed at understanding what constitutes cellular stress, how cells respond to such stress, and the role of these responses in development and disease. We are particularly invested in figuring out the role of mRNA translation regulation during cellular stress, and use fruit flies to model various human retinal degeneration and metabolic disorders where stress response signaling is known to be crucial for disease etiology. We use a broad range of experimental approaches including imaging, genetics/genome editing, ribosome profiling, and metabolome profiling. The lab training environment collectively places high emphasis on collegiality, integrity and inclusivity. Read more at www.flystresslab.com |
| Jean-Pierre Vilardaga, PhD | jpv@pitt.edu | Project 1. Structural Basis of PTH-receptor Function. The information obtained through this research will define the structural basis by which functionally distinct ligands activate the PTH receptor a medically important G protein-coupled receptor (GPCR) regulating blood levels of calcium and phosphate ions and bone turnover. Project 2. Regulation of Parathyroid Functions by GPCRs. This project will define a new process by which heterodimerization of the calcium-sensing receptor (CaSR) and the metabotropic type B1 GABA receptor (GABAB1R) regulate PTH secretion from the parathyroid glands. Project 3. Foundational Research to Act Upon and Resist Conditions Unfavorable to Bone (FRACTURE CURB): Combined long-acting PTH. This research will define the molecular basis by which calcimimetics regulate bone formation by long-active PTH analogs. Project 4. Druggability of the PTH receptor. The goal is to identify PTHR-binding small molecule compounds via a combination of computational approaches including molecular dynamics (MD) simulations, elastic network model (ENM)-based methods, and virtual screening using structures of PTHR. 1) Molecular and cellular mechanisms of G-protein coupled receptor (GPCR) signaling; 2) GPCR signaling and function in primary cilia; 3) Receptor druggability for bone diseases. Visit Vilardaga Lab |
| Ora Weisz, PhD | weisz@pitt.edu | The Weisz lab uses biochemical, quantitative imaging, genomic, metabolic and kinetic modeling approaches in cells and animal models of disease to study the endocytic pathway of kidney proximal tubule cells. Defective regulation of apical membrane traffic in these cells leads to tubular proteinuria that can progress to end-stage kidney disease. Projects in the lab focus on (1) identifying at ultrastructural resolution the interactions between apical endocytic compartments in these highly specialized cells; (2) determining how this pathway can be modulated by physiologic and pharmacologic stimuli to cause or treat disease, (3) determining the molecular basis of genetic disorders that result in tubular proteinuria; (4) discovering how endocytosis, metabolism, and transcription are coordinately regulated in these cells; and (5) establishing additional effects of SGLT2 inhibitors, clinical game changes in the treatment of diabetes and other diseases, on kidney nephron segments. Visit our website https://weiszlab.pitt.edu for more information. |
| Matt Wohlever, PhD | wohlever@pitt.edu | Research in the Wohlever lab is focused on mitochondrial membrane biogenesis and quality control. Membrane proteins present unique challenges to the proteostasis network as they must be targeted to the correct membrane and overcome substantial thermodynamic barriers to enter and exit the lipid bilayer, all while avoiding the formation of potentially toxic aggregates. Our key research questions are: 1) How do quality control factors discriminate between bona fide substrates and functional proteins in a complex cellular environment, such as the lipid bilayer; (2) Once a substrate is recognized, what are the downstream steps that lead to resolution of proteotoxic stress; and (3) How can we leverage the resulting mechanistic insights to develop therapeutic interventions in cancer and neurodegenerative disease? We address these questions using a combination of cell biology, structural biology, and biochemistry techniques. https://wohleverlab.wordpress.com |
| Bokai Zhu, PhD | bzhu@pitt.edu | Proteostasis control in aging, metabolism and neurodegeneration, with a particular interest in nuclear speckles control of proteostasis and biological rhythms. Please visit https://www.bzhulab.com/ and follow me @LabZhu on twitter |
[updated: 09/09/2024]