PhD Program: Cell Biology & Physiology
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| 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. |
| Hagood, Jim WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
I am a Pediatric Pulmonologist. My lab studies cell phenotype regulation in the context of lung fibrosis and lung development. We use in vitro and ex vivo models, mouse models, human tissue, and multi-omic approaches to explore fibroblast phenotypes in the formation of lung alveoli and in the pathologic modeling of lung fibrosis, and explore novel therapies for lung disease. Possible Rotation Projects: Markers of mechanotransduction in lung alveolar formation (immunofluorescence, bioinformatics) |
| Rau, Christoph WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Heart failure is an increasingly prevalent cause of death world-wide, but the genetic and epigenetic underpinnings of this disease remain poorly understood. Our laboratory is interested in combining in vitro, in vivo and computational techniques to identify novel markers and predictors of a failing heart. In particular, we leverage mouse populations to perform systems-level analyses with a focus on co-expression network modeling and DNA methylation, following up in primary cell culture and CRISPR-engineered mouse lines to validate our candidate genes and identify potential molecular mechanisms of disease progression and amelioration. |
| Milner, Justin WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The overall focus of our lab is to develop new and exciting approaches for enhancing the efficacy of cancer immunotherapies. We utilize cutting-edge techniques to identify transcriptional and epigenetic regulators controlling T cell differentiation and function in the tumor microenvironment, and we seek to leverage this insight to reprogram or tailor the activity of T cells in cancer. Our group is also interested in understanding how to harness or manipulate T cell function to improve vaccines and immunotherapies for acute and chronic infections. |
| Bowser, Jessica PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We are studying tissue integrity and repair to develop innovative approaches for regenerative medicine and cancer prevention. We concentrate on highly regenerative (endometrial and intestinal) tissues and are particularly interested in how persistent inflammation influences the breakdown of biochemical pathways that oversee genome stability, stem cell plasticity, and cell adhesions and how these events influence future tissue repair and onset of disease, such as cancer. Projects employ a variety of molecular, cellular, biochemical, genetic, and machine learning techniques that span across cell culture systems, genetically engineered mouse models, and human tissues to understand the impact of acute and chronic inflammation on cell division, cytoskeletal dynamics, and DNA repair in regenerating epithelial cells. |
| Heinzen, Erin WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
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| Parnell, Scott E. WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our research focuses on the genetic and cellular mechanisms that underlie how prenatal exposure to alcohol and other drugs, such as cannabinoids, disrupt normal brain development. We use a wide variety of molecular and cell biology tools including RNA-seq (whole transcriptomic profiling), mouse transgenics, and confocal imaging to understand how drugs alter cell signaling pathways and transcriptional regulation in development. Our work also studies key regulatory pathways, such as Sonic hedgehog (Shh) and other primary cilia-mediated signals, during normal and aberrant embryonic development. |