PhD Program: Cell Biology & Physiology
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| 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. |
| Chen, Gang WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We use cutting edge technology to study pathogenesis of human pulmonary diseases including cystic fibrosis, Job’s syndrome, idiopathic pulmonary fibrosis by both human specimens, mouse genetic models, with a goal of finding the therapies. Recently, we developed a serial of lung epithelial-lineage tracing systems, providing the powerful tools for identify mechanisms of lung disease involved in post-acute sequelae SARS-CoV-2 infection, also known as “long COVID”, in collaboration with Dr. Ralph Baric’s Lab at UNC-CH. |
| 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. |
| Guardia, Charly WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The human placenta is the first organ to develop after fertilization and is the least studied! We hope to change this by using a multidisciplinary approach. From iPSC-derived trophoblasts in culture to mouse models and human placenta tissue, the Placental Cell Biology Group at NIEHS answers fundamental questions about placenta cell and developmental biology. Our lab uses a range of microscopy (cryo-EM, fluorescence), recombinant protein production, and -omics techniques. The goal of our research is to understand how autophagy controls placenta development, differentiation, and function. |
| Kim, Boa WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Endothelial cells, which comprise the innermost wall of all blood vessels, are involved in a broad range of metabolic and cardiovascular diseases that represent a global challenge with high morbidity. Endothelial cell metabolism is an active process, and altered endothelial metabolism drive disease progression. The research in my lab focuses on the molecular mechanisms of endothelial cell metabolism and how they affect cardiovascular and metabolic diseases. |
| Miller, Brian WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Miller lab is working to improve the efficacy of immunotherapy to treat cancer. We aim to develop personalized immunotherapy approaches based on a patient’s unique cancer mutations. We have a particular interest in myeloid cells, a poorly understood group of innate immune cells that regulate nearly all aspects of the immune response. Using patient samples, mouse models, single-cell profiling, and functional genomics approaches, we are working to identify novel myeloid-directed therapies that allow us to overcome resistance and successfully treat more patients. |
| Hantman, Adam PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Hantman Lab is interested in how functions emerge from network activity in the nervous system. Particularly, we study how the nervous system generates patterns of activity that control our bodies in the world. Our approach combines genetics, anatomy, physiology, perturbations, and a dynamical systems approach. |
| Thaxton, Jessica WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Thaxton laboratory studies the intersection of stress and metabolism in immune cells for applications in cancer immunotherapy. Our pursuits center around the biology of the endoplasmic reticulum (ER). We aim to define how stress on the ER defines changes in protein homeostasis, metabolic fate, and antitumor efficacy of immune subsets in human tumors. In order to pursue our goals we collaborate vigorously with clinicians, creating a highly translational platform to expand our discoveries. Moreover, we design unique mouse models and use innovate technologies such as metabolic tracing, RNA-sequencing, and spectral flow cytometry to study how the stress of solid tumors impacts immune function. Ultimately, we aim to discover new ways to restore immune function in solid tumors to offer unique therapies for cancer patients. |
| Baldwin, Katie WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Building a functioning brain requires an elaborate network of interactions between neurons and glia. We use mouse genetics, primary cell culture, quantitative proteomics, molecular biology, and super resolution microscopy to study glial cells during brain development. We are particularly interested in how astrocytes acquire their complex morphology and communicate with neighboring astrocytes, neurons, and oligodendrocytes. Furthermore, we are investigating how glial dysfunction drives the pathogenesis of brain disorders such as autism, schizophrenia, and leukodystrophy. |
| Wirka, Robert WEBSITE |
PHD PROGRAM RESEARCH INTEREST |
Our lab uses human genetics to identify new mechanisms driving coronary artery disease (CAD). Starting with findings from genome-wide association studies (GWAS) of CAD, we identify the causal gene at a given locus, study the effect of this gene on cellular and vessel wall biology, and finally determine the molecular pathways by which this gene influences CAD risk. Within this framework, we use complex genetic mouse models and human vascular samples, single-cell transcriptomics/epigenomics and high-throughput CRISPR perturbations, as well as traditional molecular biology techniques. |