Student Profiles Archive - Amgen Scholars
Here you will find information about past and present students funded through scholarships administered by the Undergraduate Research Center - Sciences. We are proud of the achievements of our research scholars.
Please click on the program year to get information about the supported students, their mentors and their research projects.
| Mr. Brandon Tsai
Name: Brandon Tsai
Home University: UCLA
Major: Molecular, Cell and Developmental Biology
Faculty Mentor: Dr. Xia Yang
Brandon Tsai is a third year Molecular, Cell and Developmental Biology major at UCLA. He joined Dr. Xia Yang's lab during the winter of his first year. The Yang lab investigates the interaction between genetic and environmental risk factors, perturbation of gene networks and molecular networks, and their effect on common metabolic diseases such as, obesity, diabetes, and coronary artery disease. The lab employs an integrative genomics and systems biology approach to analyze large molecular datasets and identify specific causal candidates within networks as targets for therapy.
Brandon's current research primarily focuses on the environmental risk factor obesogens, a class of endocrine disrupting chemicals that can induce adipogenesis and obesity, and their causal role in metabolic diseases such as cardiovascular diseases, type 2 diabetes, and obesity. One such obesogen that has captured recent attention is bisphenol A (BPA) due to its widespread prevalence in everyday products such as water pipes, food containers, bottles, toys, medical equipment, thermal paper, and electronics, making it one of the most commonly produced compounds in the world. Using the C57BL/6 mouse model treated with BPA, Brandon can observe both phenotypic and transcriptomic changes from BPA treatment. Hallmark metabolic syndrome phenotypes, including body fat composition, blood glucose, lipids, insulin, and glucose tolerance, are measured in the offspring, followed by transcriptome analyses by RNA sequencing. Construction of tissue-specific gene networks then point to key regulators that mediate the molecular toxicity of BPA as well as its effect on metabolic diseases.
| Ms. Riasat Zaman
Name: Riasat Zaman
Home University: Rutgers University
Major: Molecular Biology and Biochemistry
Faculty Mentor: Dr. Jau-Nian Chen
Riasat Zaman is a rising senior majoring in molecular biology and biochemistry at Rutgers University in New Jersey. At Rutgers, she conducts undergraduate research in Dr. William Belden's lab studying the molecular mechanisms of circadian rhythms in Neurospora crassa.
As a UCLA Amgen Scholar, Riasat is working with Dr. Jau-Nian Chen in the Department of Molecular, Cell and Developmental Biology. She is studying the role of the neural crest in developing and adult hearts of zebrafish. Neural crest cells are a pluripotent cell population that migrate and assume a variety of fates through out the body. The Cardiac Neural Crest is the subpopulation of neural crest cells in the heart and has been found to play a significant role in normal cardiac functioning, and myocardial maturation; however, further understanding of its contribution still awaits investigation.
Riasat's project involves taking advantage of two transgenic lines of zebrafish that can specifically label and ablate neural crest-derived cardiomyocytes in the heart. Tracing of the cells will characterize the morphology, localization and cell differentiation fates from embryonic to adult stages of development, while ablation studies will elucidate the biological function of neural crest cells at the cardiovascular level.
Riasat would like to thank all the members of the Chen lab and the Amgen foundation for supporting her endeavors as a developing undergraduate researcher.
| Ms. Karen Wong
Name: Karen Wong
Home University: UCLA
Faculty Mentor: Dr. Jorge Torres
I am a senior majoring in Biochemistry with a minor in Biomedical Research at UCLA, where I am conducting research under the mentorship of Dr. Jorge Torres. My research focuses on characterizing two novel spindle assembly checkpoint components GGCX and CKMT1A, and identifying their roles in the context of the cell cycle.
A key objective for cell division is the equal transmission of genetic material into the two nascent cells. During mitosis, this process is highly orchestrated and it requires a complex network of signal transductions to ensure faithful chromosomal segregation. An integral member of this process is the spindle assembly checkpoint that delays the anaphase onset in the presence of DNA damage or kinetochore-microtubule attachment errors. The deregulation of SAC has been implicated in aneuploidy and tumor progression. To elucidate the precise SAC function and ultimately uncover novel chemotherapeutic drugs, we previously performed a high-throughput small interfering RNA human genome screen and identified a set of novel genes that bypassed the SAC checkpoint in the presence of Taxol, a spindle poison. CKMT1A and GGCX were among the ones we discovered. To further verify their roles in the SAC, we will knockdown these two enzymes using short hairpin RNA and observe cellular defects in fixed cells using immunofluorescence microscopy. We will also couple the knockdown to time-lapse microscopy to establish a correlation between the timing of mitotic events and the cellular phenotypes. These studies will help characterize novel proteins that regulate the cell cycle in hopes of developing targets for new cancer therapeutics.
| Mr. Andrew Takeda
Name: Andrew Takeda
Home University: UCLA
Major: Microbiology, Immunology, and Molecular Genetics
Faculty Mentor: Dr. Arnold Berk
Andrew Takeda is a rising senior at UCLA with a major in Microbiology, Immunology, and Molecular Genetics (MIMG) and a minor in Biomedical Research. Since January 2014, he has worked in the laboratory of Dr. Arnold Berk studying gene regulation by the adenoviral small e1a protein.
A hallmark of adenoviral infection is stimulation of cell cycling in the host. Because these viruses typically infect growth-arrested cells, progression through the host cell cycle allows the virus to initiate its own replication. While the viral e1a protein is known to activate cell cycling genes, recent studies have identified additional functions of e1a, including the selective repression of certain other host genes to further optimize viral replication.
This gene repression can be attributed in part to e1a's interaction with the structurally complex host transcriptional co-activator p300, which induces condensation of cellular chromatin. Andrew's current project is to further elucidate the molecular basis for e1a-mediated repression by identifying the functional domains of p300 which are involved in this condensation activity. His approach combines expression of different p300 mutants with in-vivo targeting of a fluorescently tagged e1a-lac repressor fusion to a lac operator-containing chromosome region in order to determine each mutant's capacity for condensation.
Andrew would like to thank the Berk lab, the faculty and staff of the Biomedical Research minor and URC-Sciences, and the Amgen Foundation for their guidance and support in his research pursuits.
| Mr. Ryan Rebernick
Name: Ryan Rebernick
Home University: University of Wisconsin-Madison
Faculty Mentor: Dr. Genhong Cheng
Ryan is a junior studying biochemistry at the University of Wisconsin - Madison. In Wisconsin, Ryan works with Dr. Miriam Shelef in the Department of Medicine studying the pathophysiology of rheumatoid arthritis, an inflammatory autoimmune disease. Dr. Shelef's lab seeks to understand the role of two citrullinating enzymes, PAD2 and PAD4, in the development of rheumatoid arthritis.
At UCLA, Ryan works in the Department of Microbiology, Immunology, and Molecular Genetics under the direction of Dr. Genhong Cheng studying the innate and adaptive immune response. One focus of Dr. Cheng's lab is to explore mechanisms of crosstalk between the immune and the metabolic systems. As obesity is associated with systemic inflammation, it is thought that these inflammatory pathways may contribute to obesity-related insulin resistance and type 2 diabetes among other diseases.
Adipocytes, fat cells, are an essential mechanism of organismal energy storage which are becoming increasingly known for their role within the immune system. Adipogenesis is a process traditionally thought of as strictly metabolic, but recent research in Dr. Cheng's lab suggests otherwise. Adipogenesis is coordinated primarily by the transcription factors C/EBPα and PPARγ, whose levels are controlled by another transcription factor GATA3. It is hypothesized that GATA3 levels may be regulated by other proteins important in the non-canonical NF- κB response, an inflammatory pathway. This project focuses on using CRISPR/Cas9, a genome editing tool, to selectively knockout GATA3 in preadipocyte cell lines. Creating preadipocyte GATA3 knockouts will facilitate the study of the mechanism by which the non-canonical NF- κB pathway regulates adipogenesis.
| Ms. Julie Philippe
Name: Julie Philippe
Home University: Barnard College of Columbia University
Faculty Mentor: Dr. David Teplow
Julie Philippe is a senior at Barnard College of Columbia University, majoring in Biochemistry. At Barnard, she works in Dr. Marisa Buzzeo's lab, which focuses on developing an electrochemical microRNA sensor to be used as a diagnostic tool for the detection of various types of cancers whose tumors have shown to overexpress micro-RNA genes.
This summer at UCLA, Julie is working under the mentorship of Dr. David Teplow in the Neurology Department. Dr. Teplow's lab studies the structural biology of amyloid proteins and focuses on understanding the biophysics of protein folding and assembly, especially as it relates to Alzheimer's Disease (AD). The amyloid β-protein (Aβ) has been found to play a significant role in the pathology of AD, and although formation of senile amyloid plaques formed in the brain have been pursued as the likely cause of AD, recent evidence links soluble, low-molecular weight oligomers (Aβ), monomers that self associate into 'paranuclei' onto which individual monomers attach, and their subsequent formation into protofibrils and fibrils, to the development of the disease. Therefore, the role of Aβ oligomers in the neuropathology of AD drives the need to isolate oligomers of specific order to draw structure-activity relationships. The understanding of such relationships provides key information necessary for drug development. Aβ42, one of the two predominant Aβ isoforms, is strongly linked to the neuropathogenesis of AD, but the metastability of the Aβ42 oligomers makes it difficult to isolate each oligomer species by molecular weight. The project this summer will consist of stabilizing and isolating pure populations of a variant of Aβ42 oligomers of definite order using photo-induced cross-linking of unmodified proteins (PICUP) and characterizing the pure oligomers by electron miscroscopy to determine the morphology of the oligomers, Thioflavin-T binding assays to monitor fibril nucleation activity, and circular dichroism, to determine the secondary structure of oligomers. Knowing the conformational organization of oligomers of definite order and making correlations with their biological activities will further our understanding of structure-neurotoxicity relationships of Aβ42 oligomers and will provide further knowledge applicable to a wide range of neurodegenerative disorders. Julie would like to thank Dr. Teplow, our post-doctoral mentor Dr. Eric Hayden, Joseph Conovaloff, UCLA, Dr. Tama Hasson, Dr. Patty Phelps, and the Amgen Foundation for their generous support, patience, and wisdom throughout these exciting weeks of research.
| Mr. John Ovian
Name: John Ovian
Home University: University of Connecticut
Faculty Mentor: Dr. Neil Garg
John Ovian is a rising junior pursuing an honors B.S. in chemistry with a minor in mathematics at the University of Connecticut. At UConn, he performs research in Dr. Nicholas Leadbeater's lab developing synthetic methodology using an environmentally friendly oxoammonium salt in oxidative transformations, including allyl ether cleavage, and oxidative nitrile formation from aldehydes. He has also investigated the mechanistic pathway for oxoammonium salt oxidations through a combined experimental-computational study. Additionally, John spends much of his time directing the co-ed a cappella group, Extreme Measures, and mentoring freshman honors students.
At UCLA, John is working in the Department of Chemistry and Biochemistry under the tutelage of Dr. Neil Garg on the total synthesis of tubingensin B. Over 50% of all newly discovered pharmaceutical drugs are or are derived from natural products. Indole diterpenoids such as tubingensin B often possess interesting biological properties including insecticidal, antiviral, and anticancer activities. Because of this, there is an interest in creating concise and efficient synthetic schemes that can produce these molecules in large enough quantities for biological testing.
Tubingensin B possesses a [3.2.2]bicyclic core with 5 stereocenters, two of which are vicinal quaternary centers. This presents an incredible challenge to the synthetic chemist, one which has been ameliorated by diastereospecific ring closure using an heterocyclic aryne intermediate. This transformation is the major focus of his summer research, which will be spent systematically studying the reaction to optimize efficiency and scalability.
| Mr. Alexander McQuown
Name: Alexander McQuown
Home University: University of Minnesota, Twin Cities
Major: Genetics, Cell Biology, and Development
Faculty Mentor: Dr. Margot Quinlan
Alex is a senior studying Genetics, Cell Biology, and Development at the University of Minnesota, Twin Cities. At home, Alex works with Dr. Gant Luxton studying the Linker of Nucleoskeleton and Cytoskeleton complex and its role in actin-dependent rearward nuclear positioning in migrating cells.
At UCLA, Alex works in the lab of Dr. Margot Quinlan in the department of Chemistry and Biochemistry. The Quinlan Lab focuses on studying two directly interacting actin nucleators, Spir and Capu, and how they build an actin mesh that is present in Drosophila melanogaster oogenesis and necessary for proper developmental patterning. The actin mesh is present throughout early and mid oogenesis, and disappears at the onset of a process called cytoplasmic streaming. Without Spir or Capu there is no actin mesh and cytoplasmic streaming occurs prematurely, resulting in disrupted patterning.
During the summer Alex will study how Spir and Capu are related to the regulation of organelle size. Several studies and observations have suggested that Spire may play a part in controlling the size of organelles including mitochondria, vesicles, and yolk granules. To examine this he will compare the size of various organelles in the Drosophila oocyte in wild type, spir knockout, and capu knockout flies. In addition, he will examine organelle sizes in flies expressing variants of Spir and Capu that disrupt their interaction, disrupt Spir's ability to bind actin, or inhibit Capu's ability to nucleate actin filaments.
Alex would like to thank the Amgen Foundation, Quinlan Lab, and UCLA for this opportunity.
| Ms. Erin McCaffrey
Name: Erin McCaffrey
Home University: University of Maryland, College Park
Faculty Mentor: Dr. Owen Witte
Erin McCaffrey is a fourth year Microbiology student at the University of Maryland-College Park. At home, Erin works in the laboratory of Dr. Rohan Fernandes in the Sheikh Zayed Institute for Pediatric Surgical Innovation. In Fernandes' lab she is developing a bacterial nanoconstruct to target and treat tumors.
As an Amgen scholar Erin is conducting research in the laboratory of Dr. Owen Witte of the department of Molecular and Medical Pharmacology. Under the mentorship of Dr. John Lee, Erin is investigating small molecule inhibition of Myc oncoproteins in aggressive prostate cancer subtypes. The vast majority of malignant prostate cancer occurs as acinar adenocarcinomas, which rely on androgen for survival and are typically treated with androgen-deprivation therapy. However, prostate cancer can persist after anti-androgen therapy as castration-resistant subtypes, which are aggressive and have low rates of survival. A family of transcriptional factors called Myc oncoproteins play a critical role in the growth and proliferation of these aggressive, late-stage prostate cancers. In her research Erin will investigate small molecule inhibitors that could disrupt two of these transcriptional factors, c-Myc and N-Myc, and induce toxicity across multiple prostate cancer cell lines.
The Witte lab has demonstrated that small molecule inhibitor CD532 can inhibit N-Myc expression and reduce viability in a small cell prostate cancer cell line. Erin will assess the activity of this inhibitor in c-Myc driven prostate cancer line, and identify additional small molecule inhibitors that effect N-Myc driven prostate cancer. The ultimate goal of her project is to establish potential therapeutic approaches for advanced prostate cancer.
| Ms. Katherine Liu
Name: Katherine Liu
Home University: Scripps College
Faculty Mentors: Dr. William Gelbart and Dr. Charles Knobbler
Katherine is a senior at Scripps College majoring in Chemistry and minoring in Dance. At Scripps through the Keck Science Department, she works with Dr. Babak Sanii engineering collisions between phospholipid bilayers. In addition to playing with polymers and a 3D printer, she takes image sequences using fluorescence microscopy and feeds data through computational scripts to characterize diffusion.
At UCLA, she works with Dr. William Gelbart and Dr. Charles Knobler in the Chemistry and & Biochemistry Department. Through a combination of theoretical and experimental work, the group investigates the physical basis of viral self-assembly. The genomes of many viruses are comprised of single-stranded (ss) RNA molecules that are thousands of nucleotides long. Complementary base pairing in viral-length RNAs leads to the formation of branched 2D structures, and the structure of these RNA molecules plays an important role in the way they are packaged by capsid protein and subsequently delivered into cells. Previously, the group has shown that 3D size of long RNA molecules relies heavily on secondary structure, while the distance between ends of an assembled ssRNA is independent of sequence and length.
In order to test theoretical predictions of long RNA secondary structure, Katherine's project this summer will explore poly(U), a long ssRNA molecule that cannot form base-pairing interactions with itself. She plans to optimize the synthesis of fluorescently labeled long strands of poly(U) RNA. These molecules will be assembled to determine how the 3D size of ssRNA affects its packaging into Virus-like particles.
| Mr. Mitchell Krawczyk
Name: Mitchell Krawczyk
Home University: University of Washington
Major: Neurobiology & Psychology
Faculty Mentor: Dr. Felix Schweizer
Mitchell is a rising senior at the University of Washington where he is pursuing a double major in Neurobiology and Psychology. At UW he works in Dr. Martha Bosma's lab where he studies a pattern of spontaneous activity found in the embryonic mouse hindbrain and its potential implications on neural development. At UCLA, Mitchell is working in Dr. Felix Schweizer's lab with a focus on ubiquitin's role in synaptic transmission.
Ubiquitin is a small peptide that can be covalently bound to many cellular proteins. Though it was first known to induce proteasomal degradation, recent research has suggested ubiquitin's role in modifying protein function. Prior work in the Schweizer lab suggests that ubiquitin binds to many proteins that are vital to the release of neurotransmitters. Furthermore, applying drugs that block the addition or removal of ubiquitin from target proteins changes certain aspects of synaptic transmission. For example, ubiquitination and deubiquitination blockers increase mini potential frequency in neuronal culture as well as acute slices. Interestingly, the same drugs decrease evoked response in culture but not in slices.
To address this discrepancy, Mitchell's project will explore the hypothesis that modulatory neurotransmitter systems present in slices (and not in culture) produce these different responses. He will apply adrenergic agonists or antagonists to both cultures and slices and observe the responses via whole cell patch clamp. These results will help elucidate the pathways by which ubiquitination affects synaptic transmission, a biological process that is vital to the function and plasticity of the nervous system.
Mitchell is pictured with his lab mentor.
| Ms. Caroline Jia
Name: Caroline Jia
Home University: UCLA
Faculty Mentor: Dr. Larry Hoffman
Caroline Jia is a fourth year Neuroscience major at UCLA. She has been working in the Vestibular Neuroscience Laboratory since October 2013 under Dr. Larry Hoffman and postdoctoral fellow, Dr. Peihan Orestes. She is currently studying mitochondrial compromise and potential protective mechanisms in an in vitro SH-SY5Y cell system.
During chemotherapy treatments, cisplatin is the main drug used to target soft tissue tumors. However, because cisplatin also affects inner ear sensory systems, limitations are placed on the use of cisplatin to limit ototoxic damage. Although it is already well known that high dosages of cisplatin induce apoptosis, little is known about the outcome of low dosages of cisplatin. It has been found by our lab that low dosages of other ototoxic agents induce sensory loss without inducing widespread apoptosis. Therefore, this study focuses on the mechanism of low dose cisplatin treatments and potential protection mechanisms. This study is testing to see if cisplatin induced toxicity acts by targeting the mitochondria within the inner ear and opening the mitochondrial permeability transition pore (mPTP) and causing oxidative stress. Protective drugs, including cyclosporin A, which target the mPTP have been successful in reducing drug-induced cytotoxicity. Therefore, with the coadministration of cisplatin and cyclosporin A, this study tests if low doses of cisplatin cause mPTP induction in SH-SY5Y mitochondria. In order to quantify mitochondrial response to cisplatin induced oxidative stress, three mitochondrial markers are being used: superoxide dismutase 2 (SOD2), CHCHD3, and MitoTracker. These markers are analyzed using immunohistochemistry and confocal laser scanning microscopy.
| Ms. Nisha Gopal
Name: Nisha Gopal
Home University: University of Michigan
Faculty Mentor: Dr. Jeffrey Abramson
Nisha is a rising senior at the University of Michigan (UM) in Ann Arbor. She studies biochemistry and is passionate about research and science education. At UM, she works in Dr. Ann Miller's lab in the Molecular, Cellular & Developmental Biology Department. The Miller Lab studies cell division and cell adhesion in Xenopus epithelium. Her work involves techniques including microinjection and fluorescence confocal microscopy.
Nisha is a summer Amgen Scholar at UCLA in Dr. Jeff Abramson's lab in the Department of Physiology. The Abramson lab does protein crystallography of membrane channels and transporters using a unique bicelle-based crystallography method. The lab aims to understand the molecular basis for transmembrane transport processes. The human Sodium-Galactose Transporter (hSGLT) serves as a target for the treatment of diabetes and obesity, and the lab seeks to better understand its structure and affinity for drug binding. The lab has recently solved the crystal structure of the bacterial homologue of hSGLT in Vibrio parahaemolyticus (vSGLT). Interestingly, the same drug that blocks transport in the human protein, fails to do so in the bacterial protein. Nisha's project hypothesizes that the reason for failure in drug binding of vSGLT is due to key differences in active site residues of hSGLT and vSGLT. Her summer project involves generating mutant constructs of the bacterial transporter to mimic the human transporter, and measuring affinity for the drug. A drug-sensitive vSGLT could ultimately serve as a model for further studies in drug development for the treatment of diabetes and obesity.
| Ms. Marilyn Day
Name: Marilyn Day
Home University: Ursinus College
Major: Biology with a minor in Neuroscience
Faculty Mentor: Dr. Michael S. Levine
Marilyn is a rising senior at Ursinus College where she studies biology and neuroscience. At Ursinus, Marilyn works in Dr. Jennifer Round's laboratory to investigate nervous system development. Her research specifically focuses on Slitrk1's regulation of Rohon Beard neuron populations during early spinal cord development of the zebra fish.
As a UCLA Amgen Scholar, Marilyn is working in Dr. Michael Levine's laboratory under the supervision of Dr. Laurie Galvan in the department of Psychiatry and Biobehavioral Sciences to study Huntington's disease (HD). HD is a progressive neurodegenerative disorder characterized by massive degeneration of medium spiny neurons (MSNs) in the striatum. MSN activity is locally regulated by a network of striatal inhibitory interneurons, including GABAergic parvalbumin-expressing interneurons, which regulate feed forward inhibition to MSNs.
The laboratory has previously found that optical activation of parvalbumin-expressing interneurons causes greater GABAergic responses in MSNs in mice with a severe form of HD (R6/2) than in control mice, but not in the Q175 mouse model, which have a less severe form of HD. It is hypothesized that there are other neurotransmitters that modulate MSN neurotransmission in less severe forms of HD that are able to mask or compensate for the defects observed in R6/2 mice, allowing Q175 mice to maintain relatively normal GABAergic activity. In this study we utilize optogenetics, electrophysiology and pharmacology to examine the communication between parvalbumin-expressing interneurons and MSNs in Q175 and control mice. We are investigating the potential roles of the cannabinoid system, presynaptic GABAergic receptor system, and histaminergic system in modulating GABAergic functioning in Q175 mice.
| Ms. Jamie Cyr
Name: Jamie Cyr
Home University: Smith College
Faculty Mentor: Dr. Jerome Zack
Jamie is a rising senior at Smith College working toward a major in mathematics, minor in chemistry and a concentration in biomathematics. She has worked previously with Professor Nessy Tania of Smith College on developing a mathematical model to describe and simulate breast cancer metastasis through actin regulation. Jamie has also spent time working with Professor Philip Maini of Oxford University where she modeled the dynamics of the crypt and villus system prior to the initiation of colorectal cancer.
Under the direction of Dr. Jerome Zack and Dr. Deirdre Scripture-Adams of UCLA, Jamie is working to introduce a novel and efficient way of developing T-cells from human embryonic stem cells (hESCs). She hopes to employ a mutant murine fetal organ culture (mFTOC) to achieve a high yield of T-committed cells from hESC derived hematopoietic stem cells (HSC). The mutation will cause thymic hyperplasia and provide a larger T cell niche. The hyperplasic thymus will be depleted of all murine thymocytes and recolonized with the hESC derived HSCs. The transgenic thymus will culture the HSCs for 20-40 days. She hopes to then analyze the cells for T-commitment via flow cytometry. Their work in developing a novel way of producing T-cells from human embryonic stem cells will contribute directly to the development of various T-cell therapies to treat diseases such as cancer or AIDs.
Jamie would like to thank the Zack Lab and the Amgen Foundation for their continued support in her pursuit of research excellence.
| Ms. Hannah Bell
Name: Hannah Bell
Home University: UCLA
Major: Microbiology, Immunology, and Molecular Genetics
Faculty Mentor: Dr. Peter Bradley
Hannah Bell is a 3rd year Microbiology, Immunology, and Molecular Genetics major with a minor in Biomedical Research at UCLA. She works in Dr. Peter J. Bradley's lab studying Toxoplasma gondii, an important pathogen that primarily affects immunocompromised individuals and neonates. T. gondii belongs to the phylum Apicomplexa, a group of intracellular, obligate parasites that infect large populations, both animal and human. The two most significant apicomplexan parasites affecting humans are T. gondii and its close relative Plasmodium falciparum, the causative agent of malaria. T. gondii infects about a third of the human population and can cause extensive neurological, ophthalmological and neonatal issues.
Hannah's project focuses on the Inner Membrane Complex (IMC), an organelle anchored to the parasite cytoskeleton that provides a scaffold for the parasite's replication.
While the IMC has been shown to have a role in parasite invasion, replication and motility, many of the proteins involved with this process are not known. Hannah's project will focus on characterizing several IMC proteins' function through the CRISPR/CAS9 knockout system. In addition, she plans to explore protein interaction networks through the recently published BioID method. Ultimately, Hannah hopes to study IMC proteins' phenotypes in order to identify potential drug or vaccine targets to counteract or prevent Toxoplasmosis.
Hannah would like to express her gratitude to every member of the Bradley lab, the Biomedical Research faculty, and the Amgen Foundation for their generous support of her undergraduate research and science education.
| Ms. Meghan Bell
Name: Meghan Bell
Home University: Binghamton University
Major: Integrative Neuroscience
Faculty Mentor: Dr. Albert Lai
Meghan is a fourth-year undergraduate at the State University of New York at Binghamton majoring in Integrative Neuroscience. She has experience at her home institution researching alternative methods of drug delivery in cancer treatment under Dr. Ming An of the Chemistry department. At UCLA, she has been working in Dr. Albert Lai's lab of the Neurology department researching genetic mutations in the development and recurrence of glioblastoma multiforme, a form of primary brain cancer.
Glioblastoma multiforme is the most common and aggressive form of brain cancer affecting patients today. The current approach for treatment involves surgical resection of the tumor, followed by radiation and chemotherapy. Temozolomide (TMZ) is the chemotherapeutic drug most often administered to patients and works by causing severe damage to the cancer cell's DNA, thus inducing apoptosis, or programmed cell death. While patients will initially respond to TMZ treatment, they will eventually develop a resistance to the drug. It has been found that hypermutation, a phenomenon in which a vast amount of mutations accumulate on the genome, allows for the development of this resistance.
The adenomatous polyposis coli (APC) and mutator-S homolog 6 (MSH6) proteins are consistently found to be mutated following TMZ-treatment, suggesting that these two proteins may play a key role in the development of TMZ-resistant hypermutation. Meghan plans to investigate when these two mutations occur in relation to hypermutation during TMZ treatment, hypothesizing that these two proteins mutate initially and permit the accumulation of mutations on the rest of the genome. Understanding the development of this phenomenon allows for the possible identification of new targets in cancer treatment, as well as the innovation of patient-specific treatments.
Meghan Bell is pictured with her P.I. and lab mentor.
| Mr. Thomas Aunins
Name: Thomas Aunins
Home University: Northwestern University
Major: Chemical Engineering
Faculty Mentor: Dr. Kendall Houk
Thomas "Tom" Aunins is a rising senior at Northwestern University (contrary to what his shirt in the photo suggests) studying chemical engineering with a minor in biotechnology and biochemical engineering. At Northwestern he is working with Dr. Keith Tyo of the Chemical and Biological Engineering department on BNICE, a wishfully-named computational system used for predicting novel biochemical synthesis pathways based on an organism's known metabolic reactions.
At UCLA Tom is conducting research under the guidance of Dr. Ken Houk in the Chemistry and Biochemistry department. He will be investigating the biosynthesis of the molecule fumagillin, a natural product of the fungus Aspergillus fumagatis that has a number of medicinal applications. The project will examine a section of the pathway in which a dramatic skeletal rearrangement takes place, a complex set of reactions that are believed to be catalyzed by a cytochrome P450 enzyme. Several hypotheses exist regarding the mechanism by which the P450 accomplishes this transformation, and the goal of this analysis will be to determine which of these proposals is the most favorable in terms of reaction thermodynamics and kinetics.
Tom will be applying density functional theory via the Gaussian computational program to evaluate individual structures of the minima, transition states, and side products along each pathway for their optimal conformations and molecular energies. These parameters will then be used to compare the separate proposed pathways and thus provide insight into the function of P450 enzymes, which may in turn aid future enzyme design efforts within the Houk lab.
| Ms. Emily Aguirre
Name: Emily Aguirre
Home University: California State University, Los Angeles
Faculty Mentor: Dr. Beth Lazazzera
Emily G Aguirre is a rising third year student, studying Microbiology at California State University-Los Angeles. She has been working as an undergraduate researcher under the guidance of Dr. Sunil Mangalassary, Food Science and Technology Department at CSULA, exploring the development of edible antimicrobial films using exopolysaccharides from lactic acid bacteria.
As a UCLA Amgen Scholar, she is working under the guidance of Dr. Beth Lazazzera in the Microbiology, Immunology and Molecular Genetics Department. Her project this summer consists of identifying a Competence and Sporulation Factor (CSF) binding site on ComP, a histidine protein kinase, in Bacillus subtilis.
Genetic competence in B. subtilis is regulated by extracellular signaling peptides; two of these have been identified as Competence Sporulation Factor (CSF) and ComX pheromone, each inducing a cascade reaction that activates a gene transcription factor, ComA. CSF is believed to inhibit ComA gene expression at high concentrations by binding to an unknown site though genetic evidence for the elusive, non-canonical pathway has yet to surface. If CSF inhibits ComA dependent gene expression, a binding site and a novel family of receptors for peptides involved in quorum sensing must exist.
Emily would like to thank all the members in the Lazazzera lab and the Amgen Foundation for their generous support.