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NameEmailPhD ProgramResearch InterestPublications
Hahn, Klaus
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Bioinformatics & Computational Biology, Cell Biology & Physiology, Neuroscience, Pharmacology

RESEARCH INTEREST
Biochemistry, Biophysics, Cell Biology, Cell Signaling, Chemical Biology, Computational Biology, Systems Biology

Dynamic control of signaling networks in living cells; Rho family and MAPK networks in motility and network plasticity; new tools to study protein activity in living cells (i.e., biosensors, protein photomanipulation, microscopy). Member of the Molecular & Cellular Biophysics Training Program and the Medicinal Chemistry Program.

Gupton, Stephanie
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Cell Biology & Physiology, Neuroscience

RESEARCH INTEREST
Biochemistry, Cancer Biology, Cell Biology, Cell Signaling, Genetics, Neurobiology, Stem Cells

During cell shape change and motility, a dynamic cytoskeleton produces the force to initiate plasma membrane protrusion, while vesicle trafficking supplies phospholipids and membrane proteins to the expanding plasma membrane. Extracellular cues activate intracellular signaling pathways to elicit specific cell shape changes and motility responses through coordinated cytoskeletal dynamics and vesicle trafficking. In my lab we are investigating the role of two ubiquitin ligases, TRIM9 and TRIM67, in the cell shape changes that occur during neuronal development. We utilize a variety techniques including high resolution live cell microscopy, gene disruption, mouse models, and biochemistry to understand the complex coordination of cytoskeletal dynamics and membrane trafficking driving neuronal shape change and growth cone motility in primary neurons.

Gomez, Shawn
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Bioinformatics & Computational Biology

RESEARCH INTEREST
Bioinformatics, Cancer Biology, Cell Signaling, Computational Biology, Systems Biology

Our primary research is in the area of computational systems biology, with particular interest in the study of biological signaling networks; trying to understand their structure, evolution and dynamics. In collaboration with wet lab experimentalists, we develop and apply computational models, including probabilistic graphical and multivariate methods along with more traditional engineering approaches such as system identification and control theory, to current challenges in molecular biology and medicine. Examples of recent research projects include: prediction of protein interaction networks, multivariate modeling of signal transduction networks, and development of methods for integrating large-scale genomic data sets.

Duncan, Alex
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Pharmacology

RESEARCH INTEREST
Bacteriology, Biochemistry, Cell Signaling, Immunology, Pathogenesis & Infection

My lab studies a recently identified pathogen-sensing signaling complex known as the inflammasome. The inflammasome is responsible for the proteolytic maturation of some cytokines and induces a novel necrotic cell death program. We have found that critical virulence factors from certain pathogens are able to activate NLRP3-mediated signaling, suggesting these pathogens may exploit this host signaling system in order to promote infections.  Our lab has active research projects in several areas relating to inflammasome signaling ranging from understanding basic molecular mechanisms of the pathway to studying the role of the system in animal models of infectious diseases.

Dohlman, Henrik
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Biochemistry & Biophysics, Bioinformatics & Computational Biology, Pharmacology

RESEARCH INTEREST
Biochemistry, Cell Signaling, Genomics, Pharmacology, Systems Biology

We use an integrated approach (genomics, proteomics, computational biology) to study the molecular mechanisms of hormone and drug desensitization. Our current focus is on RGS proteins (regulators of G protein signaling) and post-translational modifications including ubiquitination and phosphorylation.

Doerschuk, Claire M.
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Pathobiology & Translational Science

RESEARCH INTEREST
Cell Biology, Cell Signaling, Immunology, Molecular Medicine, Pathology

We study host defense mechanisms in the lungs, particularly the inflammatory and innate immune processes important in the pathogenesis and course of bacterial pneumonia, acute lung injury/acute respiratory distress syndrome, and cigarette smoke-associated lung disease. Basic and translational studies address mechanisms of host defense, including recruitment and function of leukocytes, vascular permeability leading to edema, bacterial clearance and resolution.  Cell signaling pathways initiated by binding of leukocyte-endothelial cell adhesion molecules and molecular mechanisms underlying the functions of neutrophils are two particular areas.

Deshmukh, Mohanish
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Cell Biology & Physiology, Neuroscience

RESEARCH INTEREST
Cancer Biology, Cell Biology, Cell Signaling, Neurobiology, Translational Medicine

We study how mammalian cells regulate their survival and death (apoptosis). We have focused our work on identifying unique mechanisms by which these pathways are regulated in neurons, stem cells, and cancer cells. We utilize various techniques to examine this in primary cells as well as in transgenic and knock out mouse models in vivo. Our ultimate goal is to discover novel cell survival and death mediators that can be targeted for therapy in neurodegeneration and cancer.

Der, Channing
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Cell Biology & Physiology, Genetics & Molecular Biology, Pharmacology

RESEARCH INTEREST
Cancer Biology, Cell Biology, Cell Signaling, Genetics, Translational Medicine

Our research centers on understanding the molecular basis of human carcinogenesis. In particular, a major focus of our studies is the Ras oncogene and Ras-mediated signal transduction. The goals of our studies include the delineation of the complex components of Ras signaling and the development of anti-Ras inhibitors for cancer treatment. Another major focus of our studies involves our validation of the involvement of Ras-related small GTPases (e.g., Ral, Rho) in cancer. We utilize a broad spectrum of technical approaches that include cell culture and mouse models, C. elegans, protein crystallography, microarray gene expression or proteomics analyses, and clinical trial analyses.

Damania, Blossom
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Genetics & Molecular Biology, Microbiology & Immunology

RESEARCH INTEREST
Cancer Biology, Cell Signaling, Pathogenesis & Infection, Translational Medicine, Virology

The work in our laboratory is focused on understanding the molecular pathogenesis of Kaposi’s sarcoma-associated herpesvirus (KSHV), an oncogenic human virus. KSHV is associated with several types of cancer in the human population. We study the effect of KSHV viral proteins on cell proliferation, transformation, apoptosis, angiogenesis and cell signal transduction pathways. We also study viral transcription factors, viral replication, and the interactions of KSHV with the human innate immune system. Additionally, we are developing drug therapies that curb viral replication and target tumor cells.

Cox, Adrienne
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Cell Biology & Physiology, Pharmacology

RESEARCH INTEREST
Cancer Biology, Cell Biology, Cell Signaling, Molecular Biology, Molecular Medicine

Our lab is interested in molecular mechanisms of oncogenesis, specifically as regulated by Ras and Rho family small GTPases. We are particularly interested in understanding how membrane targeting sequences of these proteins mediate both their subcellular localization and their interactions with regulators and effectors. Both Ras and Rho proteins are targeted to membranes by characteristic combinations of basic residues and lipids that may include the fatty acid palmitate as well as farnesyl and geranylgeranyl isoprenoids. The latter are targets for anticancer drugs; we are also investigating their unexpectedly complex mechanism of action. Finally, we are also studying how these small GTPases mediate cellular responses to ionizing radiation – how do cells choose whether to arrest, die or proliferate?