Students Supported by the T-32 Training Grant
current t-32 training grant
Graduate Student, Ihrie laboratory
BS, Georgia Institute of Technology (2017)
Graduate Student, Sappington laboratory
BS, University of Tennessee-Knoxville (2014)
previous t-32 training grant
Graduate Student, Galli laboratory
BA, Princeton University (2011)
Disruptions in dopamine (DA) homeostasis are associated with several neuropsychiatric disorders, including attention deficit hyperactivity disorder, and drug addiction. The Galli Lab has recently identified several missense mutations in the human DA transporter (DAT) gene (SLC6A3) in individuals with autism spectrum disorder (ASD). These mutations result in aberrant DAT function, strongly implicating disruptions in DA transport as a risk factor in ASD. My Ph.D. work will focuses on understanding the contributions of altered or disrupted dopamine signaling mediated by variations in DAT to ASD risk.
Graduate Student, Hong laboratory
BS, James Madison University (2015)
Hi, my name is Joe Balsamo and I grew up in Flemington, New Jersey before moving to Castle Rock, Colorado. I received my B.S. in Biotechnology from James Madison University in 2015. Following graduation, I worked for LabCorp performing clinical diagnostics for women’s health before attending Vanderbilt University. Currently, I work in the Hong lab studying zebrafish development, drug discovery, and cardiovascular biology. Outside of lab, I enjoy exploring Nashville’s food scene and attending hockey games.
Graduate Student, Meiler laboratory
BA, Colgate University (2011)
I use computational modeling and biophysical techniques to understand how proteins interact with their binding partners such as small molecules, peptides, or large proteins. The Meiler Lab actively develops the Rosetta software for protein structure prediction. I complement this software with biophysical techniques such as X-ray crystallography, nuclear magnetic resonance (NMR), and electron paramagnetic resonance (EPR). I have a particular focus on G-protein coupled receptors (GPCRs). I am interested in how ligand binding induces a conformational change in the receptor to lead to activation and signaling through cellular binding proteins such as heterotrimeric G-protein and arrestin.
Graduate Student, Sweatt laboratory
BS, Virginia Polytechnic Institute (2015)
My name is Ben Coleman and I grew up in the small town of Abingdon Virginia. I did my undergraduate training at Virginia Tech, after which I worked as a lab technician in the Department of Psychiatry at UTSouthwestern for a year before coming to Vanderbilt in the fall of 2016. I recently joined the lab of Dave Sweatt where my research will focus on the epigenetics of memory. In my free time I love to hike, fish, and spend time with my wife and dog.
Graduate Student, Blind laboratory
BA, Fisk University (2015)
It is established that the phosphatase and tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) is mutated in a variety of cancers, often resulting in PTEN loss of function. At cell membranes, PTEN opposes the activity of phosphatidylinositol 3-kinases (PI3Ks), which generate the signaling lipid PIP3. PI3K activation leads to the stabilization of key cell signaling complexes at the membrane via PH-domain mediated interactions with PIP3. This complex formation is required for proper signal transduction to occur; however, upregulated PI3K activity (overproduction of PIP3) is associated with several cancer types . However, drugs targeting membrane PI3Ks have widely failed. Our lab studies a nuclear PI3K called IPMK (inositol polyphosphate multikinase) that converts PIP2 to PIP3 while bound to a transcription factor, NR5A1. IPMK conversion of PIP2 to PIP3 while bound to NR5A1 increases the expression of NR5A1 target genes. PTEN, in an opposing manner, is able to dephosphorylate PIP3 to PIP2, causing repression of NR5A1 target genes. I hypothesize that a close NR5A1 homolog, NR5A2, is regulated by IPMK in the same way and that PIP3 stabilizes transcriptional complexes via PH-domain mediated interactions similar to its role at cell membranes. If proven, these results would implicate IPMK as a cancer drug target.
Graduate Student, Zhang laboratory
BS, Rhodes College (2011)
I study the impacts of secretase inhibition on the trafficking of amyloid precursor protein (APP) and its cleavage products. γ- and β-secretase inhibitors prevent the production of amyloid β from APP and have been investigated as possible treatments for Alzheimer’s disease. However, little is known about the potential consequences of disrupting the amyloidogenic cleavage pathway at the cellular level. I am using a dual-tagged fluorescent APP fusion protein (pH-APP-BFP2) to track APP’s subcellular distribution, endo/exocytosis and cleavage to investigate the effects of α-, β- and γ-secretase inhibitors in live primary neurons. My project aim is to increase understanding of Alzheimer’s disease pathogenesis and aid in the discovery of safer and more selective treatments for Alzheimer’s disease.
Graduate Student, Davies laboratory
BS, York College of Pennsylvania (2015)
My research focuses on the lipid signaling molecules and how these are altered by obesity. Specifically, how obesity causes a reduction in circulation of N-acylethanolamines (NAE). NAEs have been shown to have anorexic effect and reduce feedings and alter weight gain. We investigate the cellular and molecular mechanisms responsible for production of NAEs which include precursor synthesis and enzymatic production, through a combination of cellular and animal models utilizing a range of molecular and instrumental techniques. In our laboratory we also develop recombinant bacteria to alter the gut microbiome as a potential therapeutic treatment for obesity
Graduate Student, Denton laboratory
BS, University of Arizona (2014)
Diabetes affects more than 9% of Americans and has a cost burden of $245 billion. Kir4.2 (KCNJ15) was recently identified as a type 2 diabetes mellitus (T2DM) susceptibility gene and that knock down of the gene stimulated insulin secretion, a function that is normally disrupted in diabetes patients. Together, these data show that Kir4.2 is a potential therapeutic target for T2DM. I will use pharmacological tools to investigate Kir4.2 and its role on insulin secretion in in vitro models, as well as in vivo models. My project will use a range of techniques from molecular biology to integrative physiology.
Graduate Student, Conn and Niswender laboratories
BS, Miami University (2014)
My project focuses on validating novel treatment strategies for Rett syndrome and MECP2 Duplication syndrome. These are two debilitating neurodevelopmental disorders that are caused by either a loss-of-function mutation or duplication of the MECP2 gene, which codes for the transcriptional regulator Methyl-CpG-Binding Protein 2. We have shown that expression of the metabotropic glutamate receptor 7 (mGlu7) is altered downstream of changes in MECP2 gene dosage. I am particularly interested in understanding how mGlu7 function is altered in these disease contexts and to evaluate the therapeutic potential of fine-tuning mGlu7 activity with small molecule allosteric modulators. To do this, I perform genetic and pharmacological manipulations in mouse models of Rett syndrome and MECP2 Duplication syndrome using a combination of techniques that include biochemistry, brain slice electrophysiology and rodent behavior.
Graduate Student, Arinze laboratory (Meharry Medical College Student)
BS, Univ. of Nevada, Las Vegas (2006)
Graduate Student, Patel Laboratory
BA, Vanderbilt University (2013)
The Patel lab investigates the relationship between endocannabinoid signaling and stress-induced neuroadaptation. By understanding the molecular, structural, and physiological adaptations in endocannabinoid signaling that occur in response to stress, we hope to uncover novel bio-markers and pharmacological targets for drug development. My project will focus on investigating the role of endocannabinoid signaling in social interaction and social stress.
Graduate Student, Osheroff laboratory
Pharm.D., Lipscomb University (2014)
BA, Reinhardt College (2010)
Fluoroquinolones, which target type II topoisomerases in bacteria, are one of the most widely prescribed antibacterials in the world; however, resistance is on the rise. My project focuses on characterizing two new classes of antibacterials that target type II topoisomerases in bacteria: Novel Bacterial Topoisomerase Inhibitors and Mycobacterium tuberculosis gyrase inhibitors. My work will aid in antibacterial drug development to help combat fluoroquinolone resistance in a wide range of bacteria including, Escherichia coli, Neisseria gonorrheoae, and Mycobacterium tuberculosis.
Graduate Student, Wang laboratory (Meharry Medical College Student)
BS, Murray State Univ. (2013)
Graduate Student, Schoenecker laboratory
BS, Ohio Northern University (2003)
Trauma-induced skeletal muscle calcification is a spectrum of disease, including dystrophic calcification and heterotopic ossification (HO), that may occur following severe injuries such as burn, blast, neurologic and musculoskeletal injuries, as well as certain orthopaedic procedures. Under normal physiologic circumstances, when the body undergoes injury, innate protection mechanisms inhibit the formation of calcification within skeletal muscle. Additionally, the body also possesses mechanisms to remove mineral deposits formed in damaged tissues, thereby allowing for proper tissue healing and regeneration. The goal of my project is to identify critical skeletal muscle protection mechanisms and the mechanisms by which calcification is regressed from damaged tissues. Through identifying the mechanism at work, I am now examining novel therapeutics aimed at enhancing these mechanism to better prevent soft tissue calcification.
Graduate Student, Knollmann laboratory
MS, University of Connecticut (2011)
BS, University of Connecticut (2010)
Shan is a mentee in the Bjorn Knollmann lab in VanCART. Here, he is growing his toolbox for studying calcium handling and its relevance to cardiomyocyte dysfunction in models which develop cardiomyopathy and/or arrhythmias. His main project involves developing the use of iPSC-CM for modeling cardiac laminopathy.
Graduate Student, Winder laboratory
BS, York College of Pennsylvania (2013)
My research focuses on understanding the role of adrenergic signaling within the extended amygdala in stress-induced relapse of cocaine seeking. Stress is often cited as a precipitating factor in cocaine relapse. Compounds that decrease stress and anxiety by targeting adrenergic receptors, such as beta-blockers and alpha 2a adrenergic receptor agonists, show some efficacy in clinical trials. However, the neuronal substrates responsible for the beneficial effects of these compounds remains unknown. To address this gap in knowledge I am using a combination of behavioral pharmacology, genetic, and biochemical approaches to investigate the role of adrenergic receptors in the extended amygdala in cocaine and stress-exposed animals treated with adrenergic ligands.
Graduate Student, V. Gurevich and Iverson laboratories
BS and BA, Wittenburg University (2014)
Nicki is under the co-mentorship of Dr. Gurevich and Dr. Iverson, whose labs she officially joined in April 2015. Her chosen thesis research, which is to elucidate the interaction of arrestin-3 with the mitogen-activated protein kinases (MAPKs), is based on evidence from both labs and current publications in the field. As a member of two labs, Nicki is presented with the unique opportunity to approach her scientific questions from two angles: biochemical assays, which allow her to conduct studies of arrestin function, and macromolecular X-ray crystallography, which she uses to determine different arrestin complex structures. This arrangement enables her to develop novel functional experiments with the help of solved crystal structures, a process that usually requires extensive collaboration. It also exposes her to a wide variety of experimental techniques, which range from basic molecular and cell biology to advanced instrumental study.
Lab Websites:
(Gurevich) https://medschool.vanderbilt.edu/gurevich-lab/
(Iverson) https://medschool.vanderbilt.edu/iverson-lab/
Graduate Student, Hasty laboratory
BS, University of Richmond (2013)
Our lab studies the intersection of metabolism and immunology, with an emphasis on how obesity-related inflammation impacts metabolic disease progression. For my project, I am studying relationship between complement factor 5 of the innate immune system and insulin receptor processing and resultant insulin signaling. We have evidence that this protein is necessary for proper insulin action, so I am working to determine how the pathways are connected to ensure metabolic homeostasis.
Graduate Student, Blakely laboratory
BS, University of Vermont (2012)
My research explores the molecular underpinnings of serotonin transporter (SERT) regulation. More specifically, I am building on the discovery of multiple, functional SERT coding variants in subjects with autism spectrum disorder (ASD) that display altered regulation through PKG and p38 MAPK-linked pathways. The availability of a mouse model expressing the most common of these variants, SERT Ala56, provides a key opportunity to examine how disrupted SERT function and regulation leads to risk for ASD and other disorders associated with perturbed serotonin signaling.
Graduate Student, Lindsley laboratory
BSLAS, University of Illinois @ Urbana (2015)
The Lindsley laboratory focuses on drug discovery with an emphasis on the development of allosteric modulators for the validation and investigation of novel targets and mechanisms for a variety of different diseases. My project is on the development of novel and selective positive allosteric modulators for the metabotropic glutamate receptor subtype 7 (mGlu7). My primary goals are the chemical synthesis and optimization of the modulator as well as the exploration of the role of mGlu7 in the neurological disorder, schizophrenia. These studies may not only lead to a better understanding of the biology of mGlu7 in schizophrenia, but also in other neurological disorders.
Graduate Student, N. Brown laboratory
MS, Northern Arizona University (2012)
BS, University of Arizona (2009)
My research focuses on leveraging electronic health records and genetics to enhance our understanding and treatment of resistant hypertension. By identifying patients within Vanderbilt’s BioVU that have resistant hypertension we intend to test specific genetic variants to potentially identify a novel antihypertensive therapeutic. I am also using the population to determine if there are genetic predictors that predispose patients to attenuated responses to specific antihypertensive therapies.
Graduate Student, Weaver laboratory
Pharm.D., Lipscomb University(2016)
There is currently an unmet need to identify more selective drugs for Slack-induced epilepsies. In order to better understand the role Slack plays in childhood epilepsies we need to develop highly selective molecular probes. When identified, such probes will allow for the investigation of the hypothesis that selective small molecule modulators that normalize inhibitory interneuron based transmission will safely and effectively correct the epileptiform behavior caused by Slack mutations. Discovery and characterization of such compounds will provide a starting point for the development of new clinical tools for the treatment of Slack-induced epilepsies.
Graduate Student, Hadjfrangiskou laboratory
BS, Florida State University (2014)
My research is driven by an interest in antibiotics, infectious diseases, and cellular signaling. My thesis work focuses on understanding the signaling networks that Uropathogenic E. coli use throughout pathogenesis to acquire vital nutrients, respond to hazards, and to regulate virulence factors, with an overarching goal to develop new antimicrobial therapies targeting these systems.
Graduate Student, Wang laboratory
BS, Texas Southern University (2012)
The primary goal of the Wang lab is to identify mechanisms of therapeutic resistance and to translate this knowledge into transformative and effective treatments for a variety of cancers. My cancer of interest, glioblastoma multiforme (GBM), is the most malignant form of primary brain cancer with a patient life expectancy of only 12-15 months. Knowing this, my long term goal is to identify novel combination therapies that suppress or inhibit the ability of GBM tumors to self-renew, proliferate rapidly, and resistant chemo-radiation.
Graduate Student, C. Niswender laboratory
BS, Chaminade University of Honolulu, HI (2016)
I'm originally from the Philippines but grew up in the island of Oahu in Hawaii. I attended Chaminade University of Honolulu where I double majored in Biochemistry and Forensic Science. I’m interested in studying and targeting signaling pathways associated with neurodevelopmental disorders for therapeutic discovery. I have joined the lab of Colleen Niswender and Jeff Conn to pursue this interest, focusing on the implications of metabotropic glutamate receptors in the cognitive phenotypes observed in MeCP2-associated diseases, Rett Syndrome and MecP2-duplication syndrome. Outside of lab, I enjoy outdoor activities and sports, especially hiking and playing basketball.
Graduate Student, Arinze laboratory (Meharry Medical College Student)
BS, Howard University (2002)
Graduate Student, Denton laboratory
BS, University of Evansville (2016)
I was born and raised in Evansville, IN, where I received my BS in Neuroscience from the University of Evansville in 2016. Following graduation, I came directly to Vanderbilt the following fall. I am currently a graduate student in the laboratory of Dr. Jerod Denton, where I will be pursuing my interests in exploring the therapeutic potential of underexploited ion channel drug targets in the central nervous system. Outside of the lab, I enjoy fishing, hiking, and exploring the music scene.
Graduate Student, Hamm laboratory
BS, University of California, San Diego (2010)
Regulation of neurotransmitter release by activated Gi/o-type G-protein coupled receptors (GPCRs) is of relevance to not only normal brain function and but also to neural disease, such as anxiety, depression, and working memory deficiency disorders. From various known mechanisms, I am particularly interested in Gbg, one of the essential signaling units of activated GPCRs, and their interaction with soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE). Using biophysical and biochemical approaches such as a quantitative mass spectrometric targeted multiple reaction monitoring, I intend to elucidate the in vivo expression and localization of neuronal Gb and Gg subunits, and Gbg specificity to auto- and hetero a2a adrenergic receptors and SNARE.