Research Interest: Metabolism
Name | PhD Program | Research Interest | Publications |
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Tamir, Tigist WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Systems Metabolism and Signaling Lab Oxidative stress, a byproduct of energy production essential for all living organisms, arises from an imbalance of reactive oxygen, nitrogen, and carbonyl species (ROS/RNS/RCS). These highly reactive molecules present a significant waste management challenge within cells. Through evolution, oxidative stress response (OSR) pathways have emerged as critical guardian of cellular homeostasis, adept at neutralizing potentially harmful reactive molecules. Dysregulation of OSR—whether due to insufficient or excessive capacity to resolve oxidative damage—is a hallmark of numerous human diseases. For example, cancer cells co-opt OSR pathways by rewiring signaling and metabolism which leads to the development of resistance to chemotherapy. The Systems Metabolism and Signaling Lab (i.e. Tamir Lab) seeks to unravel the biochemical intricacies of how cells defend against oxidative stress by investigating the cell signaling-mediated regulation of metabolism. We aim to address fundamental questions about the biochemistry of OSR regulation, including:
To tackle these questions, we employ a multidisciplinary approach that integrates biochemistry, proteomics, metabolomics, molecular biology, and systems biology. Our work focuses on dissecting the regulatory networks governing OSR and identifying targetable pathways implicated in obesity and cancer. As a member of the Lineberger Comprehensive Cancer Center, Department of Nutrition, and Computational Medicine Program, we bridge molecular insights with systems-level understanding as we strive to illuminate novel and effective strategies for therapeutic interventions. The Systems Metabolism and Signaling Lab is committed to fostering a collaborative, creative, and diverse group that is invested in mutual growth. |
Miller, Colette WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our research investigates the effects of air pollutants on maternal health, paternal health, and the health of their children. Through the use of genomics, metabolomics, and proteomics, we investigate the molecular underpinnings of diseases following exposures to pollutants during sensitive life stages. We have broad interests across many tissue systems and diseases relevant to fertility and pregnancy. Our work also explores the Developmental Origins of Health and Disease hypothesis, investigating risks of metabolic diseases in offspring following maternal or paternal exposures to pollutants. |
van Rooyen, Lara |
PHD PROGRAM RESEARCH INTEREST |
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Travis, Kanesha |
PHD PROGRAM RESEARCH INTEREST |
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Schmidt, Annalee |
PHD PROGRAM RESEARCH INTEREST |
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Lee, Craig WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Craig Lee, Pharm.D, Ph.D. is a professor in the UNC Eshelman School of Pharmacy’s Division of Pharmacotherapy and Experimental Therapeutics (DPET). A key aspect of DPET’s mission is to optimize drug therapy through translating experimental and clinical pharmacology discoveries into precision medicine and accelerating application of these discoveries to improve patient care. Dr. Lee is trained as a clinical/translational pharmaceutical scientist with expertise in cytochrome P450 metabolism, cardiovascular experimental therapeutics, and precision medicine/pharmacogenomics. He is an active member of the UNC McAllister Heart Institute and UNC Program for Precision Medicine in Healthcare, and has an adjunct faculty appointment in the UNC School of Medicine’s Division of Cardiology. The overall objective of Dr. Lee’s research program is to improve the understanding of the central mechanisms underlying inter-individual variability in drug response as a means to develop novel therapeutic strategies that will improve public health. A major scientific focus of the Lee laboratory is the metabolism of drugs and eicosanoids by the cytochromes P450 enzyme system. The major therapeutic area of application of their research is cardiovascular and metabolic disease. The Lee laboratory seeks to identify and elucidate the key factors that exacerbate inter-individual variability in the metabolism of and response to drugs currently on the market, and determine whether implementation of genomic and biomarker-guided drug selection and dosing strategies can reduce this variability in metabolism and response and improve patient outcomes. The Lee laboratory also seeks to develop a thorough understanding of how cytochrome P450-derived eicosanoids (bioactive lipid mediators of arachidonic acid) regulate hepatic and extra-hepatic inflammatory responses, and determine whether modulation of this pathway will serve as an effective anti-inflammatory and end-organ protective therapeutic strategy for cardiovascular and metabolic disease. Using genomics and biomarkers, the lab seeks to translate their preclinical discoveries into humans and determine which subsets of the population may be most likely to respond to the therapeutic strategies under evaluation in the laboratory. The Lee laboratory is a highly collaborative and translational research program that integrates mechanistically-driven rodent and cell-based preclinical models with observational and interventional clinical studies. They have received funding from the National Institutes of Health and American Heart Association, authored over 100 manuscripts and over 100 abstracts in the areas of cytochromes P450, eicosanoid and drug metabolism, pharmacogenomics, and experimental therapeutics. Dr. Lee has served as the major research advisor for over 40 graduate students, post-doctoral fellows, and professional students. |
Bartelt, Luther WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our lab performs translational investigations of nutritional and microbiota determinants of host-pathogen interactions. We use gnotobiotic techniques (eg. germ free) mice to investigate complex microbe-microbe interactions in the context of host malnutrition, a common but poorly understood global health problem. Specific pathogens we model include Giardia (a ubiquitous parasite with unclear mechanisms of pathogenesis) and other intestinal parasites and multi drug resistant Enterobacterales (eg. Klebsiella). We work with several collaborators to translate findings in experimental models to outcomes in human cohorts. Emerging projects include determinants of host immune responses to mucosal viral infections and vaccines (eg. Polio and SARS-CoV-2). |
Hwang, Janice PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
My group is interested in understanding the effects of obesity and diabetes on the brain, particularly related to cerebral function and energetics. We conduct physiology based, mechanistic human and rodent studies to investigate fundamental questions such as how does the brain sense various nutrients (sugar, fat, etc), how does metabolic disease, sleep, aging impact brain function and metabolism? Using classic human metabolic techniques including hyperinsulinemic and hyper/hypoglycemic clamps coupled with advanced neuroimaging modalities including 1H and 13C magnetic resonance spectroscopy, functional MRI, and PET-CT imaging, my group has shown that glucose transport capacity into the human brain can be modified by factors such as obesity and insulin resistance as well as hyperglycemia, hypoglycemia and glycemic variability. We also have interests in using novel human imaging modalities to understand how obesity and diabetes impact neuroinflammation and neurodegeneration. |
Edwards, Whitney PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our lab aims to identify the fundamental molecular mechanisms underlying heart development and congenital heart disease. Our multifaceted approach includes primary cardiac cell culture, genetic mouse models, biochemical/molecular studies, and transcriptomics. Additionally, we employ proteomics-based methods to investigate 1) protein expression dynamics, 2) protein interaction networks, and 3) post-translational modifications (PTMs) in heart development. Current research projects focus on investigating the function of two essential PTMs in cardiogenesis: protein prenylation and palmitoylation. |
McCauley, Heather WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The McCauley Lab is interested in how the food we eat changes our physiology. Rare, nutrient sensing cells in the intestine called enteroendocrine cells secrete hormones in response to environmental cues that orchestrate systemic metabolism. How these cells regulate their neighbors in the gut is not well understood. We use mouse models which lack enteroendocrine cells and human pluripotent stem cell derived intestinal organoids to discover new roles for these master metabolic cells in the regulation of intestinal physiology and function. Enteroendocrine cells are dysregulated in inflammatory bowel disease, type 2 diabetes, and obesity, and loss of enteroendocrine cells results in malabsorptive diarrhea with poor survival. Our research has the potential to improve human health for a wide segment of the global population. |