Current Trainees

Alan Tung

Department of IDP's- Cancer Biology
Long Lab 

 

Benjamin Kraemer

Department of Chemical and Systems Biology 
Mochly-Rosen Lab 

 

Lisha Ou

Department of Chemistry 
Dassama Lab 

 

Nicolas Robalin 

Department of Chemistry 
Wender Lab 

 

Owen McAteer 

Department of Chemistry 
Wender Lab 

 

Rebecca Chan 

Department of Chemical and Systems Biology 
Li Lab 

 

Past Trainees

Alexandria Van Elgort

Department of Chemical and Systems Biology
Jarosz Lab 

Prions represent stable, dominant, yet reversible phenotypic states that often mimic phenotypes caused by mutation but are transferred by the cytoplasm or nucleoplasm opposed to the segregated genetic material. A screen performed by the Jarosz lab to identify protein-based forms of inheritance discovered >40 new prion proteins in the fungal species Saccharomyces cerevisiae. There is an enrichment among these proteins for genes that affect DNA replication, repair, and chromosome segregation. Interestingly, the dysfunction of many of these proteins is linked to cancer in mammals. My work in Daniel Jarosz’s lab focus on the impact prion acquisition causes to genome stability. I am investigating if prion acquisition promotes mutagenesis, genome instability, and potentially evasion of checkpoints that limit proliferation.

 

Jacob Moon Hyung Kim

Department of Chemical and Systems Biology
Skotheim Lab 

My interests lie in the system used by cells to sense and control cell size. Yeast and mammalian cells modulate the length of their G1 phases depending on their size. Cells smaller at birth have longer G1 phases to allow for sufficient growth before entering S phase, while cells larger at birth have shorter G1 phases. Specifically, I am studying the protein Bck2 in S. cerevisiae . While Bck2 is involved in regulating cell size, the underlying mechanisms are unknown. By using a combination of quantitative ChIP-seq experiments and live-cell microscopy, I aim to gain a better understanding the cell size-dependent effects of Bck2.

Lucero Rogel

Department of Molecular and Cellular Physiology
Goodman Lab

For centuries, humans have relied on plants to treat a wide range of diseases, including those that affect the central nervous system (CNS). Extracts prepared from the roots of Valeriana officinalis, commonly referred to as valerian, are used to treat sleep disorders, restlessness, and anxiety. The therapeutic effects ascribed to valerian root extracts arises from the presence and synergy of secondary metabolites (SMs), compounds synthesized by the plant to persist in its environment. Moreover, valproic acid (VPA), a compound derived from valerian, is widely prescribed as an anticonvulsant and mood-stabilizing drug for the treatment of epilepsy and bipolar disorder, respectively. The mechanisms by which valerian root SMs and VPA exert their therapeutic effects are poorly understood. A better understanding as to how these compounds engage with key players of the CNS will provide insights for the development of new therapeutics to treat a variety of mental illnesses. In the Goodman lab, the goal of my thesis project is to identify the molecular targets involved in detecting valerian root SMs and VPA. To achieve this task, I am utilizing the nematode C. elegans as a bioassay and genetic tool.  

Luis Rios

Department of Chemical and Systems Biology
Mochly-Rosen Lab

The aim of my thesis is to develop a novel peptide inhibitor. In the Mochly-Rosen Lab, we derive biologically active peptides from protein sequence and evolutionary conservation information. We currently have promising lead peptides that target the MiD proteins, little understood mitochondria-regulating proteins that seem to be involved an array of biological processes including cell survival, proliferation, and metabolism. Once validated, these new inhibitors will help us understand the role MiD proteins play in physiology and the potential utility of this type of inhibitor in disease. 

Veronica Li

Department of Chemistry
Long Lab

In the Long lab I utilize a multidisciplinary approach that includes chemistry, mass spectrometry, and mouse genetics to study the biochemical pathways of metabolic disease. Currently I am focusing on studying intermuscular adipose tissue (IMAT) which has been linked to insulin resistance, increased inflammation, as well as muscle dysfunction. Despite these associations, little is known regarding how accumulation of IMAT might lead to these phenotypes. Therefore, I aim to characterize this tissue and probe its function as a secretory organ to elucidate the factors secreted by IMAT and investigate its mechanism of action. This goal is significant because these studies may uncover novel therapeutic targets to combat the negative effects associated with IMAT.

Joydeb Sinha

Department of Chemical and Systems Biology
Bintu Lab

My current graduate research is in the lab of Mary Teruel, where I am using live, single cell fluorescence microscopy and synthetic biology approaches to study role of cell intrinsic circadian rhythms in adipogenesis (fat cell differentiation). More specifically, I am investigating how perturbations to circadian dynamics and pulsatility of naturally circadian hormones such as corticosterone affects the propensity of adipose precursor cells to differentiate into mature fat cells. Given that loss of rhythmic hormone secretion as well as circadian disruption has been associated with various forms of metabolic pathophysiology including obesity and diabetes, I hope one day this work will provide some insight toward the development of molecular therapies targeting these diseases.

 

Christina Jensen

Department of Chemical and Systems Biology
Wysocka Lab

I am conducting my thesis research in the lab of Dr. Joanna Wysocka. My project is centered on the question of what permits a genomic region to function as an enhancer. Enhancers are non-coding regulatory sequences that can induce transcription from their cognate promoter independent of distance or orientation. These elements are critical for proper development and tissue-specific gene expression. Despite much work in the field, it is still unclear what characteristics of a genomic region, be it sequence, chromatin landscape, or architecture, are required for enhancer function. This work will contribute to a better understanding of the mechanisms by which enhancers regulate gene expression, and, ultimately, will lead to novel therapeutic approaches for diseases associated with variants in regulatory elements.

Marlene Heberling

Department of Chemical and Systems Biology

Co-advised by Dr. Tom Wandless and Dr. Josh Elias

I am conducting my thesis research in the lab of Dr. Josh Elias, who specializes in using large-scale proteomics strategies to better understand many aspects of the immune system. My research focuses on determining the role of the T-cell Receptor as an antigen. Each T cell expresses a unique T-cell Receptor which could theoretically  be used to regulate T-cell responses by other immune cells  or even serve as a neoantigen in T-cell lymphomas. In my training I hope to develop skills in  proteomics and signal transduction network analysis. This work has many implications in understanding a healthy immune response, autoimmunity, and cancer which I hope to translate to therapeutics. 

Laura Keller

Department of Chemical & Systems Biology
Bogyo Lab

My research concentrates on the role of serine hydrolases in bacteria. Using activity-based probes, we can discover novel enzymes, explore their functions, and develop these probes as potential therapeutics. I am currently studying commensal bacteria in the skin like Staphylococcus epidermidis and in the gut. For example, in S. epidermidis, I am exploring the function of an esterase whose homolog in the pathogenic Staphylococcus aureus has been shown to be important in colonization. I have screened for new potent inhibitors of this enzyme and am using these inhibitors to determine the role of this homolog in S. epidermidis skin colonization in mice and identify its substrates. Understanding the factors that control S. epidermidis colonization and being able to manipulate this process with small molecule inhibitors will allow for further investigation of S. epidermidis’s interactions within the commensal skin microbiome and with the host.

Kaustabh Basu

Department of Chemistry
Glenn Lab

I am currently working to develop novel small-molecule inhibitors of host targets for use as broad-spectrum antiviral drugs with a high barrier to resistance. Using a multidisciplinary approach, I design and synthesize novel small molecules, then screen them using various in vitro biochemical and cell-based techniques. Compound design is informed by computational chemistry and structural biology. Molecules with desirable properties are then screened in vivo, and inform the design of further optimized molecules with clinical potential. The aims and techniques utilized in this project are aligned with the goals of the Molecular Phamacology grant, which emphasizes work at the interface of chemistry and biology that produces translatable discoveries.

Katie Ferrick

Department of Chemical and Systems Biology
Meyer Lab

My  research focuses on unpacking the mechanisms that allow cells to modulate their proliferation based on mechanical cues (including contact inhibition of proliferation, CIP). One major player in this process is the tumor suppressor Merlin, which integrates inputs from GFRs, cell-matrix adhesions, and cell-cell junctions and turns on CIP signaling. My project aims to establish Merlin's function in regulating proliferation, which will provide insight into how its inactivation leads to tumor growth and altered cell motility. Advances in this field will both enlighten our understanding of tissue homeostasis and identify potential targets for cancer therapeutics. 

Adriana Garcia

Department of Chemical and Systems Biology
Mochly-Rosen Lab

Glucose-6-phosphate dehydrogenase (G6PD) is the rate limiting enzyme of the pentose phosphate pathway and changes in its activity are associated with several disease states. Structurally, it is well known that G6PD is a monomer, homo-dimer, and homo-tetramer with only the latter two being active. However, it has only recently been shown that the tetramer is four-fold more efficient then the dimeric form and the significance between the dimer to tetramer interconversion has not been studied. My research aims to understand if the tetramer is physiologically significant and aims to understand how protein-protein interactions and post translational modifications influence G6PD’s oligomeric state. I would like to use the insight gained from this research to identify therapeutic strategies to modulate G6PD activity.

Hannah Moeller

Department of Chemical and Systems Biology
Annes Lab

I am conducting my thesis work in the lab of Justin Annes, who is an expert in cell signaling, pharmacology, and high throughput screening in the context of b-cell biology. I have embarked in a project investigating the regulatory pathways that control b-cell identity and insulin secretory function. I am working through both a pilot chemical screen and a genome-wide screen in collaboration with the Michael Bassik lab to identify signal transduction networks and genetic systems critical to this important phenotype, which may elucidate novel therapeutic strategies for diabetes. From this training, I believe I will develop the skills necessary to reach my ultimate goal to become a researcher that interrogates cell signaling pathways with the objective of identifying intervention points that address human disease.

Zachary Harvey

Department of Chemical and Systems Biology
Jarosz Lab

My work centers on understanding the fundamental molecular mechanisms underlying epigenetic inheritance driven by conformational transitions of intrinsically disordered. My primary areas of work are understanding the molecular events fueling robust conformational switching events, the consequent rewiring of transcription and chromatin landscapes following such events, how distinct cell identities are discriminated between during development, and how these phenomena might be dysregulated or coopted in disease states such as cancer. An exciting opportunity of this work is that it establishes new avenues for targeting and modulating the establishment and maintenance of epigenetic states, particularly in the context of human disease.

Marisa Hom

Department of Chemical and Systems Biology
Chen Lab

My research focuses on small molecule inhibitors of the Hedgehog (Hh) signaling pathway in cancer. Current small molecule therapies target the upstream pathway member Smoothened (SMO), but these drugs are effective only in subsets of Hh-driven cancers and are highly sensitive to chemoresistance. In the Chen lab, we have performed a high-throughput screen of over 300,000 small molecules and have identified a class of compounds, “glimidazoles”, that inhibit the pathway at the downstream level of GLI. I am currently exploring how glimidazoles affect metabolic functions to alter GLI activity. The Molecular Pharmacology training grant has provided me with the resources and guidance to pursue this project. 

Opher Kornfeld

Department of Chemical and Systems Biology
Mochly-Rosen Lab

Within a single mammalian cell, thousands of mitochondria form a dynamic network. Mitochondrial fission and fusion drive the dynamics of these networks. An imbalance between these two processes leads to dysfunctional mitochondria and cell damage. Therefore, mitochondrial dynamics are attractive therapeutic targets for a variety of diseases, including neurodegenerative disorders. My research approach utilizes specific rationally-designed peptides to inhibit protein-protein interactions as pharmacological tools to understand the mechanisms that regulate mitochondrial dynamics. These peptide inhibitors have clinical potential through their remarkable specificity, conformational flexibility, and ability to easily penetrate the blood-brain barrier and cell membranes.

Owen Smith

Department of Chemical and Systems Biology
Straight Lab

My research concentrates on studying mechanisms that maintain genomic integrity. During cell division the cell duplicates the genome and segregates each copy into a daughter cell. Chromosome segregation requires a single attachment point to each sister chromatid called a kinetochore. The Kinetochore is built upon the centromere, a constitutive DNA-protein complex. I am interested in understanding molecular mechanisms that control maintenance of the centromeric chromatin. A better understanding of this complex problem can provide insight into how aneuploidy arises and how it can contribute to cancer formation. Importantly basic research advances in this area are potentially of interest to those hoping to develop therapeutics for cancer treatment.