Faculty | Research projects/interest | |
---|---|---|
Katherine Aird, PhD | kaa140@pitt.edu | The lab is interested in cellular metabolism and how that shapes cell fate, influences the microenvironment, and affects cancer cell therapeutic response. Any projects that fall into that large umbrella would be considered. I tailor rotation projects based on scientific interests. |
Jonathan Alder, PhD | jalder@pitt.edu | The Alder lab studies the impact of telomere length on human health and disease. Currently we have three project that need graduate students! 1. Testing a novel therapy to lengthen telomeres in patients with genetic defects that cause premature telomere shortening. 2. Investigating novel telomere-related genes that were identified in a genome-wide CRISPR screen 3. Characterizing a novel mouse model of pulmonary fibrosis caused by telomere dysfunction. |
Daniel Altschuler, PhD | altschul@pitt.edu | Combination of biochemistry and imaging/optogenetic approaches in cell signaling. |
Gavin E. Arteel, PhD | gearteel@pitt.edu | 1. Degradome in ALD 2. Role cysteine proteases in NASH fibrosis 3. ECM microvesicles in ALD |
Jonathan Beckel, PhD | jmbeckel@pitt.edu | Research in the Beckel Laboratory focuses on the physiological/pathophysiological control of the urinary bladder, with a particular focus on how the urothelium acts as a sensor and interacts with bladder afferent nerves to drive bladder urgency and/or pain. Additional projects include elucidating the neurotransmitters responsible for neuromodulation of bladder sensations by tibial, hypogastric or pudendal nerve stimulation, and the mechanisms involved in inducing bladder inflammation though urothelial lysosomal signaling, and the role of cholinergic signaling in bladder cancer. |
Juliane Beier, PhD | JIBEIER@pitt.edu | Research focuses on interactions of environmental chemical exposures and lifestyles that increase risk of chronic liver disease and which may be preventable. The Beier lab has demonstrated that low doses of VC that are not overtly hepatotoxic, may serve as a contributing factor in the development and progression of liver disease and cancer and is now working on the underlying mechanisms. Current available projects include: 1. What are the mechanisms of the interaction between exposure and liver disease? Elucidating and analyzing mitochondrial dysfunction, organelle miscommunication and epigentetic/epitranscriptomic changes. 2. What are the mechanisms by which low level VC can promote tumor formation and enhance carcinogenesis? 3. Can we prevent/predict/treat this interaction? This would include pharmacologic or genetic interventions in cell culture and animal models. |
Yuri Bunimovich, MD, PhD | yxbderm1@pitt.edu | Research projects include: 1. Neuroimmune regulation of melanoma and non-melanoma skin cancer progression. These studies focus on understanding how sensory neurons and Schwann cells contribute to cancer progression and metastasis, specifically via immunomodulatory mechanisms. 2. Pathogenesis of lipid redox dysregulation in the inflammatory skin diseases. These studies explore novel signaling mechanisms of dysregulated redox lipid products generated in keratinocytes and immune cells, and their relevance to psoriasis and atopic dermatitis. 3. Role of ferroptosis in neoplastic and inflammatory skin diseases. These studies focus on ferroptosis in different cellular compartments in cutaneous diseases and on targeting ferroptosis as a novel therapeutic approach to treat neoplastic and inflammatory skin diseases. 4. Glial functions in cancer, skin inflammation, wound healing and peripheral neuropathy. These studies focus on peripheral glial cells, abd their role in a wide range of physiological and pathological processes in the skin. |
Timothy Burns,MD, PhD | burnstf@upmc.edu | 1. Structure functional analysis of RAS hydrolysis mutations in lung cancer. 2. Mechanisms of TWIST1 mediated p27 degradation. 3. Mechanisms of HGF-dependent TWIST1 regulation during tumorigenesis and acquired resistance. 4. Identification of the mechanisms through which harmine leads to TWIST1 proteasomal degradation. 5. Development and Characterization of Harmine Analogs and Derivatives 6. How does the HGF/MET/TWIST1 pathway promote brain metastases? 7. Can we target lung cancer brain metastasis with MET/TWIST1 inhibitors. 8. Can we utilize metabolic inhibitors to overcome MET TKI resistance? 9. Can glycolytic inhibitors be effective against MET-dependent brain metastases? 10. How does TWIST1 regulate HK2 expression? |
Stephen Chan, MD, PhD, FAHA | chansy@upmc.edu | 1. Multi-omic analysis in pulmonary hypertension 2. Mechanistic analysis of a brain-lung blood vessel axis in pulmonary hypertension |
Wei Du, MD, PhD | duw@upmc.edu | 1. interplay between DNA damage and immune response in leukemia development 2. a beneficial persistent DNA damage induced immune response in aging 3. leukemia-associated macrophage specific TREM1 expression in leukemia development 4. Hematopoietic stem cell (HSC) regeneration under DNA damage repair deficiency and aging |
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 |
Oliver Eickelberg, MD, FERS,ATSF | eickelbergo@upmc.edu | 1. Progenitor cell populations in lung transplantation 2. Extracellular matrix drives fibrotic cell behavior |
Elise Fouquerel, PhD | elf115@pitt.edu | 1. Roles for PARP1 in the resolution of R-loop structures to prevent genome instability. This project will employ a variety of techniques from cell biology to single molecule assays, mass spectrometry and next gen sequencing. 2. PARP2 in the response to oxidative stress in cancer cells. Multiple sub projects are available to study the roles of PARP2 in orchestrating the response of telomeres to replications. It will require cell biology and molecular biology techniques. |
Stacy Gelhaus, PhD | gstacy@pitt.edu | 1. Murine model of asthma with NO2-fatty acid therapy 2. Nitro-fatty acid alteration of macrophage metabolism in cell culture and animal models 3. Investigation into the role of trimethylamine oxide and FMO3 in obesity-associated asthma |
Sharon George, PhD | sageorge@pitt.edu | The project will involve determining the cardioprotective effects of exercise on human and mouse hearts during cancer chemotherapy. Cardiac function and mechanistic pathways underlying sex-specific cardioprotection will be investigated. |
Aditi U. Gurkar, PhD | agurkar1@pitt.edu | Potential projects include: 1. Defining the role of a central metabolite, acetyl-CoA, in cellular senescence: We discovered that acetyl-CoA generation and compartmentalization is altered in response to persistent DNA damage (Science Advances, 2022). We look forward to hosting a graduate student interested in the intersection of metabolism, epigenetics and senescence to drive this project and discover the role of acetyl-CoA in senescence and aging. 2. The role of lipid breakdown in biological aging: We recently performed metabolomics in healthy versus rapid agers (TedX; https://www.youtube.com/watch?v=9eOofp64IYI&t=15s). Causal inferencing with machine learning approaches has identified that the breakdown of lipids in different organelles is putatively associated with accelerated aging (Aging Cell, 2024). Research initiatives will now identify if lipid breakdown is causal to biological aging using cells and mouse models. |
Nadine Hempel, PhD | nah158@pitt.edu | 1. Role and regulation of antioxidant enzyme systems in cancer. 2. Ovarian cancer cell survival adaptations during metastasis. 3. Mitochondrial redox signaling during metastasis. 4. Mitochondrial dynamics and function in tumor progression. |
Baoli Hu, PhD | baolihu@pitt.edu | 1) Studying a newly identified protein binding complex, CHI3L1-Gal3/Gal3BP, contributing to the tumor immune microenvironment in glioblastoma progression and therapy 2) Studying the role of WNT5A in controlling cell plasticity for tumor progression, recurrence, and treatment resistance in glioblastoma 3) A Studying the role of SMARCD3/BAF60C in neurodevelopment and medulloblastoma |
Yu Jiang, PhD | yuj5@pitt.edu | Cell surface presentation of G protein coupled receptors |
Michael Jurczak, PhD | jurczakm@pitt.edu | Mitochondrial quality is maintained in part by a process called mitophagy that degrades damaged mitochondria via the autophagosome. USP30 is a deubiquitinase that regulates mitophagy by reducing ubiquitination of outer mitochondrial membrane proteins. We observed that mitophagy is reduced in liver hepatocytes of obese mice and that reduced hepatocyte mitophagy contributes to the pathogenes of type 2 diabetes and metabolic dysfunction-associated fatty liver disease (MASLD). We are currently testing whether USP30 deletion or inhibition can rescue reduced mitophagy during MASLD and improve disease outcomes. |
Melanie Konigshoff, MD, PhD, ATSF, FERS | koenigshoffm@upmc.edu | 1. Role of Wnt signaling in lung disease and aging. 2. Multiomic analysis of senescence in the human lung |
Edwin Levitan, PhD | elevitan@pitt.edu | Use optics to study neuropeptide release in the fly brain that affects sleep and circadian rhythms |
Yael Nechemia-Arbely, PhD | arbelyy@upmc.edu | 1. Optimizing long-read Oxford nanopore sequencing 2. Optimizing DiMelo-seq for various applications 3. Examining the relationship of CENP-A/C/T centromere proteins at human centromeres using long-read Oxford nanopore sequencing 4. Chromosome elimination using CRISPR/Cas9 5. Single molecule approaches to detect histone PTMs |
Abby Olsen, MD, PhD | abby.olsen@pitt.edu | 1. Identifying novel glial therapeutic targets for Parkinson's disease 2. Understanding gene-environment interactions in Parkinson's disease 3. Developing models of non-motor symptoms of Parkinson's disease |
Patricia Opresko, PhD | plo4@pitt.edu | 1. Investigating the role of oxidative damage at telomeres in the alternative lengthening of telomeres pathway (ALT) in cancer cells through homology directed repair 2. Studying how inhibitors of the DNA damage response factor ATR kinase alters telomerase activity and telomere maintenance in cancer cells 3. Investigating how oxidative damage at telomeres triggers premature cellular aging and senescence 4. Developing a novel probe for detecting and measuring oxidative damage at telomeres in tissue and oxidative stress conditions and aging. |
Roderick O'Sullivan, PhD | osullivanr@upmc.edu | 1. Mechanistic analysis of Alternative Lengthening of Telomeres 2. Investigating epigenomics drivers of ALT cancer cell fate and survival 3. Killing cancer cells by targeting DNA-ADP-ribosylation 4. Interrogating the impact of DNA-ADP-ribosylation on DNA replication and repair |
Patrick Pagano, PhD | pagano@pitt.edu | Opportunities in the Pagano lab include: 1) An ongoing basic to translational research project deciphering the role of free radical-generating enzymes (particularly the NOX1) in distal cell signaling, unfolded protein response and neoplasia of vascular cells in pulmonary hypertension. 2) Preclinical testing of proprietary NOX2-selective inhibitors in neuronal and cerebrovascular dysfunction in Alzheimer's Disease, involves in vivo testing of inhibitors in mice and opportunities to use advanced imaging like 2-photon microscopy and MRI on mouse brains to observe changes in blood flow and neuronal damage. |
Michael Palladino,PhD | mjp44@pitt.edu | 1. Validating and developing lead compounds as therapies for TPI Df. 2. Examining the bioenergetic underpinnings of neuromuscular function. 3. Investigating the mechanistic basis of neurologic dysfunction in metabolic disease. |
Anita Saraf, MD, PhD | saraf@pitt.edu | 1. Evaluating the effect of various drug therapies on mitochondrial organization in cardiomyocytes from congenital heart disease patients. 2. Evaluating the effect of SGLT2 inhibitors on iPSC derived cardiomyocytes from patients with congenital heart disease 3. Evaluating dysregulation of integrins and connexins in invitro cardiac organoids derived from patients with congenital heart disease |
Francisco Schopfer, PhD | fjs2@pitt.edu | 1. Metabolism and disease: Evaluate the impact of inhibiting fatty acid oxidation in cells (hepatocytes, macrophages) and therapeutic opportunities. This involves cell culture, metabolomics, lipidomics, mass spectrometry, western blot and PCR. Mechanisms used by cells to establish metabolic status: We interrogate how cells evaluate their metabolic state and rapidly respond to changes using state-of-the-art methodology including click chemistry, tagging, western blot, metabolomics and lipidomics 2. Phototherapy to treat psoriasis: We developed new reactions and mechanism that will benefit the current phototherapy approaches that patients receive. Studies include mouse work, phototherapy, mass spectrometry, and immunological assessments. |
Iain Scott, PhD | scotti2@upmc.edu | 1. Characterizing novel metabolic targets in heart failure with preserved ejection fraction (HFpEF) 2. Cardio-hepatic crosstalk in metabolic disease |
Sruti Shiva, PhD | sss43@pitt.edu | 1. Understanding the role of mitochondrial dynamics proteins in vascular remodeling/atherosclerosis 2. Elucidating the mechanisms by which platelet mitochondria contribute to thrombosis in human aging 3. Determining the role of platelet metabolism and oxidant signaling in vascular disease including scleroderma and sickle cell disease |
Thomas Smithgall, PhD | tsmithga@pitt.edu | Discovery and mechanism of action of allosteric inhibitors of tyrosine kinases involved in blood cancers; mechanism of action of novel antiretroviral drug candidates. Experimental techniques and approaches include recombinant protein expression and purification, in vitro biochemical assays, biophysical approaches including SPR and protein crystallography, and cell based assays for inhibitor action and acquired resistance. |
Wayne Stallaert, PhD | stallaert@pitt.edu | 1. cell cycle plasticity as a mechanism of drug resistance 2. cell cycle plasticity in bladder cancer heterogeneity |
Adam Straub, PhD | astraub@pitt.edu | Numerous ongoing projects are dedicated to fundamental and translational research in cardiovascular redox biology. These initiatives delve into core cellular signaling and explore their implications in conditions like hypertension, sickle cell disease, stroke, and heart failure. Additionally, there are opportunities for drug development projects within the lab. For relevant publications from the lab, you can visit the following link: https://pubmed.ncbi.nlm.nih.gov/?term=straub+ac&sort=date |
Sina Tavakoli, MD, PhD | tavakolis@upmc.edu | Development of targeted theranostic agents in inflammatory and fibrotic lung diseases. |
Jesus Tejero Bravo, PhD | jet68@pitt.edu | 1. Development of heme protein based carbon monoxide antidotes and oxygen carriers. 2. Albumin-Heme-NO complexes as vasodilators - mechanisms of endocytosis and activation of soluble guanylyl cyclase 3. Structure and function studies of novel globins – Cytoglobin, Neuroglobin, Androglobin |
Mary Torregrossa, PhD | torregrossam@upmc.edu | Neurobiological studies of substance use disorders to understand mechanisms of susceptibility and to identify therapeutics for relapse prevention. |
Bennett Van Houten, PhD | vanhoutenb@upmc.edu | Analysis of DNA repair proteins using cell biology, biochemical, and single molecule techniques |
Jean-Pierre Vilardaga, PhD | jpv@pitt.edu | 1. Structural basis of G protein-coupled receptors signaling. 2. Regulation of Parathyroid Functions by GPCRs. 3. Identification and optimization of small molecule allosteric modulators for bone and diseases, and prostate cancer metastases 4. Molecular and cellular mechanisms of endosomal cAMP signaling |
Qiming (Jane) Wang, PhD | qjw1@pitt.edu | 1. Protein kinase D (PKD) as a novel target in neuroendocrine prostate cancer (NEPC): This NIH project (R01CA229431) in collaboration with Dr. Zhou Wang and Jiaoti Huang (Duke) will determine the potential role of PKD in the pathogenesis of treatment-related NEPC, an aggressive lethal subtype of prostate cancer. The study will determine the novel role of PKD in mitotic cell cycle regulation and its impact on the development of NEPC. The PKD small molecular inhibitors developed in the Wang lab will be tested as potential therapeutic agents for this cancer. The study will be conducted both at cellular level and in mice using mouse models of prostate cancer. The work may lead to identification of novel therapeutic targets for NEPC and provide mechanistic insights to therapy resistance in prostate cancer. 2. Discovery and development of targeted therapeutics for ischemic stroke: This AHA funded project aims to identify novel potential therapeutic targets that promote neuronal survival and recovery after ischemic stroke. The current focus is on novel protein kinases and long non-coding RNAs (lncRNAs). Cell-permeable peptides or small molecules targeting these kinases or lncRNAs will be designed and evaluated using cellular and animal models of ischemic stroke. |
Wen Xie, MD, PhD | wex6@pitt.edu | Covalent modification of proteins in liver diseases (liver fibrosis and fatty liver), cancer (liver, colon, and pancreatic), and obesity and type 2 diabetes. The cell types we are interested of include hepatocytes, hepatic stellate cells, macrophages, and tumor associated macrophages. |
Cheng Zhang, PhD | chengzh@pitt.edu | Measure GPCR signaling in HEK293 cells using fluorescence-based methods. |
Hua Zhang, MD, PhD | zhangh18@upmc.edu | The Zhang lab develops the most advanced mouse models for lung cancer immunotherapy. The main research focuses of the Zhang's lab are: 1. establishing new immunocompetent mouse models for lung cancer and utilizing them to study the therapeutic efficacy and mechanisms of novel combination of targeted therapy with immunotherapy 2. identifying new therapeutic vulnerabilities to overcome drug resistance in lung cancer 3. characterizing the organ-specific tumor immune contexture to develop immunotherapeutic strategies |
Lianghui Zhang, MD, PhD | LHZHANG@pitt.edu | 1) To explore lung vascular endothelial cells as antigen-presented cells to stimulate the proliferation of T cells following influenza virus infection. 2) To identify the coronavirus (COVID-19) proteins to induce human lung vascular endothelial cell death. 3) To characterize the immune profile of endothelial-specific interferon alpha receptor knock-out mice following influenza virus infection. |
[updated: 5/22/2024]