Research Interest: Metabolism
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| Morris, John WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Morris lab leverages flexible mouse models of hard to treat cancers of the pancreas and liver to identify how cancer drivers perturb evolutionarily selected developmental programs and how such programs may be re-normalized. We focus on (1) the relationship between tumor suppressor pathways and the epigenetic determinants of cell plasticity, (2) evolutionary routes unleashed by specific tumor suppressor loss, and (3) how diversification at both the epigenetic and genomic level contribute to cancer development and therapeutic response. |
| Bryant, Kirsten WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The overall goal of our lab is to perform research that contributes to a better understanding of pancreatic cancer biology and leads to improved treatments for this disease. One major focus of our studies is the metabolic activity, autophagy, which is a self-degradation process whereby cells can orderly clear defective organelles and recycle macromolecules as a nutrient source. Current projects are focused on further advancing autophagy inhibition as an anti-RAS therapeutic approach, as well as delineating other metabolic consequences of RAF-MEK-ERK MAPK inhibition. |
| Jiang, Guochun WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Antiretroviral therapy (ART) is effective in suppressing HIV-1 replication in the periphery, however, it fails to eradicate HIV-1 reservoirs in patients. The main barrier for HIV cure is the latent HIV-1, hiding inside the immune cells where no or very low level of viral particles are made. This prevents our immune system to recognize the latent reservoirs to clear the infection. The main goal of my laboratory is to discover the molecular mechanisms how HIV-1 achieves its latent state and to translate our understanding of HIV latency into therapeutic intervention. Several research programs are undertaking in my lab with a focus of epigenetic regulation of HIV latency, including molecular mechanisms of HIV replication and latency establishment, host-virus interaction, innate immune response to viral infection, and the role of microbiome in the gut health. Extensive in vitro HIV latency models, ex vivo patient latency models, and in vivo patient and rhesus macaque models of AIDS are carried out in my lab. Multiple tools are applied in our studies, including RNA-seq, proteomics, metabolomics, highly sensitive digital droplet PCR and tissue RNA/DNAscope, digital ELISA, and modern and traditional molecular biological and biochemical techniques. We are also very interested in how non-CD4 expression cells in the Central Nervous System (CNS) get infected by HIV-1, how the unique interaction among HIV-1, immune cells, vascular cells, and neuron cells contributes to the initial seeding of latent reservoirs in the CNS, and whether we can target the unique viral infection and latency signaling pathways to attack HIV reservoirs in CNS for a cure/remission of HIV-1 and HIV-associated neurocognitive disorders (HAND). We have developed multiple tools to attack HIV latency, including latency reversal agents for “Shock and Kill” strategy, such as histone deacetylase inhibitors and ingenol family compounds of protein kinase C agonists, and latency enforcing agents for deep silencing of latent HIV-1. Several clinical and pre-clinical studies are being tested to evaluate their potential to eradicate latent HIV reservoirs in vivo. We are actively recruiting postdocs, visiting scholars, and technicians. Rotation graduate students and undergraduate students are welcome to join my lab, located in the UNC HIV Cure Center, for these exciting HIV cure research projects. |
| Flick, Matthew PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our laboratory studies the role of the blood coagulation system in inflammatory, infectious, and malignant disease. Specifically, we are interested in better defining the roles of factors such as prothrombin, fibrinogen and plasminogen in driving disease processes in the contexts of pancreatic ductal adenocarcinoma (PDAC), Staphylococcus aureus infection, and obesity/metabolic syndrome. Current studies suggest that coagulation factors drive mechanisms of disease both dependent and independent of their traditional roles in hemostasis and thrombosis. Our overall goal is to translate this knowledge into novel approaches for treating these common yet deadly diseases. |
| Dowen, Rob WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Appropriate allocation of cellular lipid stores is paramount to maintaining organismal energy homeostasis. Dysregulation of these pathways can manifest in human metabolic syndromes, including cardiovascular disease, obesity, diabetes, and cancer. The goal of my lab is to elucidate the molecular mechanisms that govern the storage, metabolism, and intercellular transport of lipids; as well as understand how these circuits interface with other cellular homeostatic pathways (e.g., growth and aging). We utilize C. elegans as a model system to interrogate these evolutionarily conserved pathways, combining genetic approaches (forward and reverse genetic screens, CRISPR) with genomic methodologies (ChIP-Seq, mRNA-Seq, DNA-Seq) to identify new components and mechanisms of metabolic regulation. |
| Jensen, Brian WEBSITE |
PHD PROGRAM RESEARCH INTEREST |
Our lab uses cell culture and animal models to define the mechanisms that lead to heart failure and to identify novel approaches to its treatment. We are particularly interested in the roles of inflammation and cardiomyocyte metabolism in the pathobiology of the failing heart. Ongoing projects focus on (1) the cardioprotective role of the alpha-1A adrenergic receptor; (2) transcriptional regulation by the nuclear receptor ROR-alpha; (3) cardiotoxicity of antineoplastic kinase inhibitors. |
| Nagarajan, Shanmugam WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The main goal of the Nagarajan lab research program focuses on how the innate branch of the immune system regulates adaptive immunity, as it relates to the pathogenesis of autoimmune disease such as lupus or rheumatoid arthritis (RA)-induced cardiovascular disease. IgG-Fcgamma receptor (FcgR)-mediated signaling is critical for mediating host defense against infectious disease, but they also mediate disease pathology in autoimmunity and atherosclerosis. Specifically, we are studying the role of IgG-Fcgamma receptor (FcgR) signaling network in innate immune cells activation that contributes to autoantibody production and T cell subset activation associated with autoimmune, and cardiovascular diseases. We are using a repertoire of relevant knockout mouse and humanized FcgR mouse models to address the questions of how FcgR-mediated signaling promotes autoimmune disease-induced atherosclerosis. As a translational component, we are collaborating with rheumatologists and cardiologists to analyze changes in innate and T cell subsets in patients with lupus or RA, who has premature atherosclerosis. |
| Shaikh, S. Raza WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Shaikh lab aims to understand how differing dietary fatty acids regulate outcomes associated with immunity and metabolism in the context of obesity, type 2 diabetes, and cardiovascular diseases. The lab conducts studies at the human level and in mouse models. We are currently focused on the mechanisms by which omega-3 fatty acids improve chronic inflammation and humoral immunity upon viral infection in obesity. We are also elucidating how select fatty acids disrupt the biophysical organization of the inner mitochondrial membrane of differing cell types and thereby respiratory activity. |
| Lorenzo, Damaris N. WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Cytoskeletal-associated proteins are critical for the maintenance of cellular homeostasis, and their involvement in cancer and in numerous neurodegenerative, neurodevelopmental, psychiatric, heart, muscular, and metabolic disorders underscores their functional relevance. Our lab investigates the contribution of the cytoskeleton to key physiological processes and the mechanistic basis of cytoskeleton-associated disorders. Our goal is to understand the roles of cytoskeletal proteins in the regulation of cellular dynamics and bioenergetics in metabolically active tissues as well as their involvement in brain development and connectivity. Our initial efforts focus on the ankyrin and spectrin families of cytoskeletal-associated proteins, which deficits have direct implications in the regulation of cell migration, in metabolic disorders such as obesity and diabetes, and may also underlie neurological diseases, including spinocerebellar ataxias, autism and West syndrome. We combine human genetics, cellular and biochemistry approaches with Omics technologies and high resolution imaging-based assays in primary cells and in animal models of development and human disease. |
| Gershon, Timothy R. WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
As a pediatric neurologist and brain tumor researcher, I seek to understand the link between brain growth and childhood brain tumors. My lab focuses on in vivo studies of the normal process of postnatal neurogenesis and the pathologic process of brain tumor growth, using mice genetically engineered to develop medulloblastoma. Our in vivo approach allows us to study how metabolism, apoptosis regulation and cell cycle control contribute to development and tumor formation. Through a long-term collaboration with Drs. Alexander Kabanov and Marina Sokolsky in the Eshelman School of Pharmacy, we are using insight from tumor biology to develop new, nanoparticle-delivered treatments for medulloblastoma, which we then test in our in vivo models. Most recently, we have used single-cell transcriptomic analysis (scRNA-seq) to understand how these treatments impact brain tumors, growing in vivo. |