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The Undergraduate Research
Scholars Program

2007-2008

Mr. Mansoor Arain
Ms. Sandy Chang
Mr. Gordon Chen
Ms. Natalie Chen
Mr. Ted Chen
Ms. Tyffany Chen
Ms. Emily Chien
Mr. David Chu
Ms. Ruby Chung
Ms. Thu Doan
Mr. Peter Edpao
Mr. Andrew Fithian
Mr. Manuel Hakimi
Mr. Thomas Hanff
Mr. George Hanna
Mr. Robert Hanna
Ms. Faranak Hassanzadeh
Ms. Mary Haviland
Ms. Tuyet Ho
Mr. Kin Wai Hung
Mr. Nate Jacobs

Mr. Mansoor Arain
Mentor: Dr. Dan S. Ray
Funding: Alcott Scholar
Title: Purification and Characterization of a Protein Complex Required for Cycling of mRNA Levels in Crithidia fasciculata

Mansoor Arain is a fourth-year undergraduate student majoring in Molecular, Cell, and Developmental Biology (MCDB) with a minor in Near Eastern Languages and Cultures (NELC). Taking advantage of the plethora of research opportunities that UCLA has to offer, he first began working in a research laboratory during his freshman year. He has been a member of Dr. Dan S. Ray’s Microbiology, Immunology, and Molecular Genetics laboratory since Winter 2005.

Dr. Ray’s lab is dedicated to the study of kinetoplastids, with a particular emphasis on kDNA replication and on kinetoplastid gene regulation. Crithidia fasciculata and Trypanasoma brucei, the latter of which causes African sleeping sickness, are the two main protozoans being studied.

Mansoor is currently working on a project to elucidate the regulation of gene expression in Crithidia fasciculata. Unlike in most other organisms, gene regulation in C. fasciculata is post-transcriptionally, not pre-transcriptionally, moderated. CSBPII, an RNA-binding protein complex, is known to be involved in this regulation, but the actual composition of this complex has not yet been conclusively determined. Appropriately, Mansoor is attempting to purify and characterize the complete CSBPII protein complex.

Mansoor will be graduating from UCLA in Spring 2008. He is currently in the process of applying to medical school, and hopes to pursue a career in academic medicine. He would like to thank Dr. Dan S. Ray for giving him the opportunity to do scientific research, and the Rosalind Alcott Estate for supporting and encouraging this interest.

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Ms. Sandy Chang
Mentor: Dr. Stephen Young
Funding: Boyer Scholar
Title:
Characterization of lamin B1 and lamin B2 proteins

Sandy Chang is a fourth-year Molecular, Cell, and Developmental Biology major with a minor in French. She works in Dr. Stephen Young’s laboratory and has been involved in the study of lamin proteins since her first year at UCLA.

The nuclear lamina is a thin intermediate filament meshwork lying underneath the inner nuclear membrane of the cell’s nucleus. Its major components are the lamin proteins, which are essential for maintaining the structural integrity of the nucleus and are separated into type A and B lamins. Two type B lamins are lamins B1 and B2. LmnB1 knockout mice have revealed that lamin B1 is a crucially important protein. The knockout mice die late during embryonic development or shortly after birth. There has been very little research on lamin B2. Sandy is currently investigating the relationship between the lamin B1 and lamin B2 proteins. At the cellular level, Sandy has already shown that lamin B1–deficient cells have more misshapen nuclei than lamin B2–deficient cells, as judged by immunofluorescence microscopy. She has also shown through western blotting analysis that cells lacking either lamin B1 or lamin B2 do not compensate for the missing one type B lamin by producing more of the other lamin protein. This suggests that lamins B1 and B2 are regulated independently of each other. Further studies will involve the generation of compound heterozygous and double knockout mice of both lamin B1 and lamin B2.

Sandy would like to thank Dr. Young and everyone in Young Lab for all of their guidance and support throughout the years. She would also like to extend her gratitude to the UCLA URC/CARE Center and the Albert C. Boyer Estate for supporting her research.

 

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Mr. Gordon Chen
Mentor: Dr. Genhong Cheng
Funding: Boyer Scholar
Title:
Characterizing the functional domains of MEKK1


(from left to right): Erin Tricker, Gordon Chen, Dr. Genhong Cheng

Gordon Chen is a fourth-year Microbiology, Immunology, and Molecular Genetics major at UCLA. Since the summer after his second year, he has been conducting research in Dr. Genhong Cheng’s lab. Under the mentorship of graduate student Erin Tricker, Gordon is studying the protein MEKK1, a mitogen-activated protein kinase kinase kinase, and its role in initiating apoptosis by cancer chemotherapeutics.

Tumor formation arises from unregulated proliferation and resistance to cell death or apoptosis. These proliferation abnormalities are targets for anticancer drugs by inducing apoptosis through DNA damage. DNA damage-induced apoptosis is regulated by the tumor suppressor gene, p53. However, because p53 activity is lost in as many as 50% of all cancers, these tumors are resistant to DNA damaging drugs. Thus to combat these p53 deficient cancers, drugs such as microtubule inhibitors such as vinblastine and paclitaxel are important in the fight against cancerous cells that have a mutated p53 gene. It is known that these drugs disrupt the dynamic nature of microtubules which leads to the malfunction of mitotic spindles during cell division. This disruption leads to both cell cycle arrest and apoptosis, yet the pathways by which these drugs induce apoptosis are not well characterized. Understanding the mechanism by which these drugs elicit an apoptotic response may improve our ability to fight cancer. Our laboratory has previously shown that MEKK1 is essential for apoptosis induced by microtubule-disrupting agents but the mechanism of this pathway remains unclear. The focus of Gordon’s project is to identify novel functional regions of the MEKK1 protein through random mutagenesis. This study will hopefully help reveal the function of MEKK1, which may help in elucidating the mechanism by which microtubule inhibiting drugs cause apoptosis.

After graduating, Gordon hopes to attend medical school. Gordon would like to thank the scholarship fund for their generosity, and would also like to thank Dr. Genhong Cheng, Erin Tricker, and the Cheng lab for their guidance, support, and passion for discovery.

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Ms. Natalie Chen
Mentor:
Dr. Oliver Hankinson
Funding: Bonner Scholar
Title:
Protective Effect of Selective Aryl Hydrocarbon Receptor Modulators (AHR) Against Breast Cancer

Natalie Chen is a fourth year Physiological Science major at UCLA and has been working since September 2006 as a member of the Hankinson lab in the department of Pathology and Laboratory Medicine. Under the guidance of Dr. Oliver Hankinson and Erin Hsu, she has been studying the chemoprotective effects of non-toxic aryl hydrocarbon receptor modulators (AHR) against breast cancer. Specific non-toxic AHR modulators which can be obtained through human diet are used in order to assess the down-regulation of the genes that play a central role in the metastasis of breast cancer. By treating human breast cancer cell lines with phytochemicals such as diindolylmethane (DIM), genistein, phenethyl isothiocyanate (PEITC), and sulphoraphane, the goal is to demonstrate the down regulation of mRNA expression through RT-PCR analyses for the G-protein coupled receptor CXCR4 and its unique ligand CXCL12. The CXCR4 and CXCL12 gene are under investigation because disruption of the CXCR4/CXCL12 axis has been shown to limit the metastasis of breast cancer cells to the lung in mice. In addition to this work, she is also investigating the necessary dosages of various phytochemical combinations which optimally down-regulate CXCR4 and CXCL12 expression, thereby providing maximal chemopreventive benefits. The results of this project may provide important clinical insight into the chemopreventive effects of dietary phytochemicals and other AHR modulators.

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Mr. Ted Chen
Mentor: Dr. Jake Lusis
Funding: Alcott Scholar
Title:
Genomewide gene expression profiling to identify genes and metabolic pathways affecting complex diseases including atherosclerosis, diabetes, and insulin resistance

Ted Chen is a fourth year undergraduate student majoring in Biochemistry. After spending a summer working at the City of Hope Beckman Research Institute under Dr. Fong Fong Chu, Ted was introduced to Dr. Jake Lusis and his laboratory at UCLA. For the past year, Ted has been working for Dr. Jake Lusis under Dr. Richard Davis.

The Lusis lab is interested in the genetics of common diseases, and the lab is currently focused on variations in gene expression in mouse and human populations. The aim of this is to gather phenotypic as well as gene expression data to identify genes that are correlated to certain disease traits. The analysis of these genes is done through expression quantitative trait loci (eQTL) analysis. For most of his time at the lab, Ted has worked using a variety of analytical tools to derive biologically significant information from the vast quantities of data generated from such experiments. In addition to his work analyzing and interpreting array data, Ted will also measure a number of mouse phenotype parameters including body mass, metabolic rate, and blood pressure.

Ted plans on pursuing a career in medicine after graduating from UCLA. He would like to thank the Alcott Estates for their generous scholarship, and the URC/CARE, Dr. Jake Lusis, and Dr. Richard Davis for their gracious support and guidance.

 

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Ms. Tyffany Chen
Mentor: Dr. Fuyuhiko Tamanoi
Funding: Honorary URSP
Title:
Identification and Characterization of Putative GEF for Rheb in S. Pombe

(from left to right) P.J. Aspuria, Tyffany Chen, and Dr. Fuyuhiko Tamanoi

Tyffany Chen is a third year student majoring in Microbiology, Immunology, and Molecular Genetics. She joined Dr. Fuyuhiko Tamanoi’s lab in the summer of 2006. Under the supervision of Ph.D candidate, Paul-Joseph Aspuria, Tyffany hopes to identify the putative GEF (guanine nucleotide exchange factor) in the critical Tsc/Rheb/TOR signaling pathway that is involved in regulating cell growth and cell cycle progression. Rheb is a GTP-binding protein that is conserved from yeast to human. The Tsc1/Tsc2 complex has been shown to function as a GAP (GTPase activating protein) for Rheb that significantly decreases the ratio of Rheb GTP/GDP-bound form by direct interaction. The overactivation of Rheb is a major cause of tuberous sclerosis, a genetic disorder characterized by the appearance of benign tumors called hamartomas. Several studies have contributed to the speculation that a GEF is involved in the reverse shuttling of Rheb from a GTP-bound form to its inactive GDP-bound form. Tyffany has narrowed a list of S. Pombe GEF candidates to one candidate complex. She has carried out experiments with several titratable promoter strains that exhibit regulated GEF overexpression in the presence of thiamine. Currently, she uses western blotting and immunoprecipitation to check the interaction of Rheb and the putative GEF.

Tyffany is extremely grateful to her mentor, Dr. Tamanoi for his guidance and for giving her the opportunity to contribute to his research lab. She is also thankful for the patience and continual support of PJ Aspuria. Tyffany hopes to attend medical school and continue her research endeavors. She would like to thank the Undergraduate Research Center for providing such a vast resource of opportunities to enable students to reach for a deeper understanding of science.

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Ms. Emily Chien
Mentor: Dr. Lianna Johnson, Dr. Steve Jacobsen
Funding: Van Trees Scholar
Title:
The characterization of SUVH4/KYP homologs, SUVH5 and SUVH6, in epigenetic regulation of Arabidopsis thaliana

(from left to right) Dr. Steve Jacobsen, Emily Chien, Dr. Lianna Johnson

Emily Chien is a fourth year Molecular, Cell and Developmental Biology major and has been conducting research under the guidance of Dr. Lianna Johnson and Dr. Steve Jacobsen. Her current research project focuses on epigenetic regulation of histone methyltransferases SUVH5 and SUVH6 in Arabidopsis thaliana. Epigenetic regulation involves the methylation and modification of DNA and histones. In plants, three known DNA methyltransferases are Methyltransferase 1 (Met1), Domains Rearranged Methylase (DRM2), and Chromomethylases (CMT3). In the Arabidopsis genome, sites of DNA methylation have been known to be associated with histone H3K9 methylation. Her project will be investigating homologs of KRYPTONITE (SUVH4/KYP) with the aim of clarifying their roles and associations in epigenetic regulation. SUVH4/KYP has been shown to be the major H3K9 MTase that is required for maintenance of non-CG methylation by CMT3. Additionally, SUVH5 has also been shown to exhibit similar histone methyltransferase behavior in vitro and maintenance of H3 mK9 and CMT3-mediated non-CG methylation in vivo. Different combinations of SUVH5 and SUVH6 with SUVH4 have been shown to mediate different regulatory activities. Maintenance and control of transposon sequences have been shown to be mediated by combined SUVH4 and SUVH5 activity whereas SUVH4 and SUVH6 activity have resulted in the control of a transcribed inverted repeat. These examples of locus specificity may indicate a relationship with CMT3 activity and provide a more conclusion picture of how DNA and histone methyltransferases interact in epigenetic regulation.

Emily would like to thank Dr. Lianna Johnson and Dr. Steve Jacobsen for their continued guidance as well as the Van Trees for their generous support.

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Mr. David Chu
Mentor: Dr. Benhur Lee
Funding: Wasserman Scholar
Title:
Cysteines in the stalk domain of the attachment protein for Nipah virus are critical for viral entry

David Chu is a fourth year Biochemistry major. He is continuing his second year of research at Dr. Benhur Lee’s lab under the guidance of Dr. Benhur Lee and Dr. Oscar Negrete. Currently, his research involves investigating the step during Nipah viral entry at which the cysteine NiV-G mutants manifest their fusion deficient phenotype. Nipah virus consists of two key envelope proteins which are necessary for viral entry, the attachment protein (NiV-G) and the fusion protein (NiV-F). Studies in other paramyxoviruses suggest that the stalk domain of the G plays a critical role in its interaction with F and possibly F-triggering, a process in which the attachment protein communicates a “signal” to F. There are three cysteines in the stalk domain of NiV-G, one or more may contribute to forming the di-sulfide linked oligomers of G. Mutations were made in the stalk domain, changing the cysteine residues to serine residues, resulting in the inhibition of fusion when co-express with NiV-F in fusion permissive cell lines. The long term goals of his research involve characterizing the properties of these cysteine mutants and consequently how these cysteines are involved in communication with the fusion protein.

David plans on attending graduate school sometime after graduating UCLA. He would like to thank Dr. Benhur Lee for the opportunity to conduct research, Dr. Oscar Negrete for his undying support and the Wasserman family for their generosity in support of this project.

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Ms. Ruby Chung
Mentor: Professor H. Thomas Hahn
and Dr. Zhanhu Guo
Funding: Bonner Scholar
Title:
Fabrication of Magnetic Metallic Nanoparticles Reinforced Polyacrylonitrile Nanocomposite

(from left to right): Dr. Zhanhu Guo, Ruby Chung, Dr. Thomas Hahn

Ruby  is a fourth year student majoring in Mechanical Engineering . She is continuing her second year of research at Dr. Hahn's lab (Multifunctional Composites Lab, MCL) under the guidance of Dr. Zhanhu Guo. 

Composites reinforced with micron-size fillers are currently used in many applications, nanocomposites reinforced with nano-scale fillers have greater efficiency due to more lightweight and have great wide potential applications in electronic devices.

Ruby has been working with iron nanoparticles, which are used in data storage, as catalysts for fabrication of carbon nanotubes or fibers, and in biomedical systems, such as MRI and site-specific drug delivery. Until now, she has learned the nanocomposite fabrication and characterization methodologies. This coming year, the main research is focusing on fabricating polyacrylonitrile nanocomposites reinforced with nickel nanoparticles. The target is to obtain high-quality composite with uniform particle dispersion and strong chemical bondage between the nanoparticles and the matrix. Various physical properties, such as thermal stability and magnetic properties of the nanocomposites will be explored.

 

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Ms. Thu Doan
Mentor: Dr. Albert Lai
Funding: Bonner Scholar
Title:
The Role of DNMT1 and DNMT3b in Glioblastoma Hypermethylation

Thu Doan is a fourth year undergraduate student majoring in Neuroscience. She has been conducting research in Dr. Albert Lai's Neuro-oncology Lab since Spring 2007. Under the guidance of Dr. Lai, she is exploring the role of DNMT1 and DNMT3b in the hypermethylation of glioblastoma.

Thu proposes to study epigenic alternations that occur in glioblastoma, one of the most aggressive types of brain tumors with a median survival of one year. One of the most important alterations in glioblastoma is DNA hypermethylation of CpG dinucleotides within promoter regions. Such promoter methylation causes gene silencing. They hypothesize is that DNA methyltransferase 1 (DNMT1) and 3b (DNMT3b) initiate the hypermethylation of CpG islands in glioblastoma. Further, they propose that DNMT1 and 3b either function in combination to initiate the abberent methylation or that one of these enzymes alone is responsible. They expect to see that DNMT1 and 3b overexpression results in the methylation of a specific set of promoter regions. This determination will help to identify novel methylated genes, signatures of coordinately methylated genes, and upstream modulators of aberrant tumor methylation. By characterizing the genes controlled by promoters with DNMT1-dependent methylation, they may be able to provide novel therapeutic approaches for glioblastoma patients.

Thu is very thankful for the help and encouragement she has received from Dr. Lai and from her mentor, Maya Remington. She could not have asked for a more dedicated lab with which to work or for a more valuable experience. Thu would like to express her gratitude to URC/CARE and Bonner for supporting her work. She plans on applying to medical school after she graduates in the Spring.

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Mr. Peter Joseph Edpao
Mentor: Dr. Guoping Fan
Funding: Wasserman Scholar
Title:
Examination of Dnmt1 Knock-Out Effects in the Mouse Brain

(from left to right) Dr. Guoping Fan, Peter Joseph Edpao, Jian Feng

Peter is a third year neuroscience major and has been working in the Depart of Human Genetics with the Fan Lab since the winter of 2007. He has spent the past year learning the various concepts and techniques required for his project, and is excited about finally getting to apply them. Working under the guidance of Jian Feng and Dr. Guoping Fan, Peter’s project will compare adult neurogenesis in wild-type and DNA methyltransferase-deficient knock-out mice.

Adult neurogenesis has been demonstrated in the subventricular zone and dentate gyrus of the mammalian brain. The specific role of DNA methylation, if any, in adult neurogenesis has yet to be elucidated. Here we examine the effects of the DNA methyltransferase (Dnmt) family of enzymes on adult neurogenesis. Specifically, we investigate the roles of Dnmt 1, crucial for the maintenance of DNA methylation patterns following cell division, and Dnmt 3a and Dnmt 3b, necessary for de novo methylation and normal embryonic development. Prior studies have shown that methyl-CpG binding protein 1 (MBD1), important for transcriptional gene repression, is associated with the promotion of normal levels of adult neurogenesis. In contrast, initial findings here indicate that knock-out mice, lacking Dnmt 1, Dnmt 1 and Dnmt 3a, or Dnmt 3a and Dnmt 3b, have increased levels of adult neurogenesis, suggesting a suppressive role for the Dnmt family in adult neurogenesis.

Peter plans to graduate UCLA in the spring of 2009 and would like to thank the Fan Lab members and Wasserman family for their guidance and support.

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Mr. Andrew Fithian
Mentor: Dr. James Gober
Funding: Boyer Scholar
Title: Characterizing the conserved chromosome partitioning proteins ParA and ParB in Caulobacter crescentus

Andrew is a fourth year Biochemistry major. He began working in Dr. Gober’s lab in 2007 under the mentorship of Arun Divakaruni.

Andrew’s current research is on the chromosome partitioning proteins of the GidPar operon, ParA and ParB. ParA, ParB and the conserved sequence ParS are required for efficient chromosome partitioning in many prokaryotic chromosomes and plasmids. ParA shows sequence homology to a family of ATPases but does not hydrolyze ATP at an appreciable rate. Instead, ParA’s function is targeted by nucleotide switching facilitated by ParB. ParB binds a specific genomic sequence ParS. The ADP bound form of ParA binds single stranded DNA and the ATP bound form stimulates dissociation of ParB from ParS. Cell cycle regulation of ParA and ParB is the main target of Andrew’s research.

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Mr. Thomas Hanff
Mentor: Dr. Thomas Minor
Funding: Waingrow Scholar
Title: Biochemical and Anatomical Substrates of Behavioral Depression

Thomas Hanff is a fourth-year pre-medical student majoring in neuroscience with a minor in public affairs. Having begun his work in the behavioral neuroscience lab of Dr. Thomas Minor three years ago, he is now embarking upon his departmental honors thesis. His project concerns the anatomical and biochemical mechanisms of behavioral depression, attempting to show that neural metabolic regulation is the ultimate source of this disease. Previous experiments in rats have indicated adenosine as a neurotransmitter that supports the autoinhibition of metabolically overactive neurons, resulting in a state of conservation withdrawal or learned-helplessness reminiscent of depression in humans. In several paradigms of depression (e.g. inescapable shock and reserpine), an injection of adenosine A2A receptor antagonists immediately ameliorates symptoms of the disease that are measurable in animals. Taking these data one step further, Thomas will test whether adenosine inhibition can be localized to the ventral medial striatum (an area rich in A2A receptors) by directly infusing adenosine A2A receptor antagonists into this portion of the brain in reserpinated rats.

This hypothesis is highly significant because it could expand our knowledge of the basic underlying biology of depression, allowing for the development of new pharmacological therapies for treatment-refractory depression. Owing to the limited efficacy of drugs developed within the prevailing monoamine theory of depression (about one-third of all 100 million depressed patients on these drugs do not improve), this would be a huge advance for the field of psychiatry.

Thomas is currently applying to medical school with the hopes of becoming a neurologist. He would like to thank Mr. and Mrs. Waingrow and the URSP program for their generous support.

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Mr. Manuel Hakimi
Mentor: Dr. Volker Hartenstein
Funding: Van Trees Scholar
Title: Genetic analysis of early hematopoiesis in Drosophila melanogaster

Manuel Hakimi is a fourth-year Molecular, Cell, & Developmental Biology major. Beginning in September of 2007 he conducted his research in Dr. Hartenstein’s laboratory under supervision of Lolitika Mandel. In his project, Manuel is focusing on understanding the gene network that is activated in the head mesoderm of the Drosophila embryo to indicate blood cell formation. The main focus of his present study is to address the question of whether or not there is a direct relationship between the repressions of tinman by buttonhead (two genes that are expressed in mesoderm) or if there are other cofactors involved in the process? Studies have been done to address long-standing issues of vertebrate biology using Drosophila in vivo studies. Using the same model, Manuel’s project of head mesoderm and hematopoiesis aims to enrich the understanding of the primitive hematopoiesis compared to its vertebrate counterpart.


Manuel is so grateful for the opportunity given to him by Dr. Hartenstein to take a part in the research project at the laboratory. He is also very thankful to Rex Van Trees Estate for their support and contribution that helped him to obtain his research and succeed in the future. In addition, Manuel is planning to apply to medical school and pursue a career in medicine.

 

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Mr. George Hanna
Mentor: Dr. Alvaro Sagasti
Funding: Honorary URSP
Title: Assessing the role of macrophages and granulocytes in the degeneration of severed trigeminal axons in zebrafish

George Hanna is a fourth-year undergraduate majoring in Molecular, Cell, and Developmental Biology. He has been working in the laboratory of Dr. Alvaro Sagasti since April 2007. His focus is on assessing the role of macrophages and granulocytes in the degeneration of peripheral axons in zebrafish.

One of the processes that have been extensively studied in zebrafish development is the growth and branching of neurons. There are many classes of neurons in the zebrafish and one class of particular interest is the trigeminal neurons. Each trigeminal neuron has two axons, one that enters the brain where it connects to other neurons, and another that branches within the skin. When the axons of these organisms are severed, the portion of the axon distal to where the cut was made degenerates rapidly (usually in less than 3 hours) in a manner reminiscent of Wallerian degeneration. As macrophages have been shown to hone to these sites of injury, our aim is to examine the role that they, and the related granulocytes (neutrophils), play in the mechanisms of this degeneration.

George is sincerely appreciative of the guidance he has received from Dr. Sagasti. He also would like to give his gratitude to URC/CARE, especially Dr. Audrey Cramer who has provided valuable insight to research-oriented career information. George is currently applying to Medical Schools.

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Mr. Robert Hanna
Mentor: Dr. Albert Lai
Funding: Van Trees Scholar
Title: Determination of effective predictors of response to the standard of care in newly diagnosed Glioblastoma patients

Robert Hanna is a fourth-year undergraduate majoring in Neuroscience at UCLA. He has been working with Dr. Lai on Glioblastoma since September 2007. His focus is on exploring biomarkers that can predict how a patient suffering from Glioblastoma will respond to the standard of care—surgery followed by chemotherapy and radiation.

Glioblastoma Multiforme (GBM) is the most common primary malignant brain tumor. It is a devastating disease complicated by the difficulty of determining which patients will respond successfully to treatment. Robert is analyzing cranial MRI scans for different pre-treatment tumor characteristics like initial tumor size, edema, and location to determine which factors most prevent a patient from being successful under the standard of care. Aside from the initial presentation of a tumor, an important feature during chemotherapy and radiation is the activity of O (6) – methylguanine-DNA methyltransferase (MGMT), one of our body’s natural DNA repair proteins. GBM often takes advantage of this molecule to heal itself in the presence of therapeutic agents. Robert is also working with the Lai lab to compare pre-treatment methylation levels of the MGMT gene between patients that are successful in treatment and those that are not. They hypothesize that patients with higher natural MGMT methylation levels will respond better to treatment.

Robert is very thankful for the nurturing, encouragement, and support he has received from Dr. Lai, Weidong, and Jana. He truly relishes his lab experience. Robert would also like to extend his sincere gratitude To URC/CARE, Cathy Knapp, and the Rex Van Trees Estate. He is currently applying to medical school.

 

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Ms. Faranak Hassanzadeh
Mentor: Dr. Osvaldo Rey
Funding: Wasserman Scholar
Title:
Identification of Protein Kinase Cs Interacting with Protein Kinase D in Living Cells Using Bioluminescence Resonance Energy Transfer

Faranak Hassanzadeh is a fifth year undergraduate majoring in biochemistry. She has been volunteering in the Department of Medicine, Division of Digestive Diseases under the guidance of Dr. Osvaldo Rey since the summer of 2006.

The goal of her project is to identify which novel isoform of protein kinase C (PKC) is interacting with protein kinase D (PKD) by using bioluminescence resonance energy transfer (BRET). This is a technique that is used to study protein-protein interactions in living cells in real time.

PKC, a major target for the potent tumor promoting phorbol esters, has been implicated in the signal transduction pathways regulating a wide range of biological responses, including changes in cell morphology, differentiation, and proliferation. There are multiple related PKC isozymes, i.e. the conventional PKCs ({alpha}, {beta} I, {beta} II, and {gamma}), the novel PKCs ({delta}, {epsilon}, {eta}, and {theta}) and the atypical PKCs ({zeta} and {lambda}).

PKD and two recently characterized serine/threonine protein kinases, termed protein kinase D2 (PKD2) and protein kinase D3 (PKD3), constitute a new protein serine/threonine kinase subfamily separate from the previously identified PKCs. PKD has been implicated in the regulation of a variety of cellular functions, including DNA synthesis and cell proliferation, chromatin modification, Golgi organization and function, c-Jun signaling, NF{kappa}B-mediated gene expression, and cell migration.

To further understand the signal transduction pathway regulated by PKD, it is crucial to identify which novel isoform of PKC is interacting with PKD.

Faranak plans to attend pharmacy school after she graduates from UCLA.

She would like to thank Dr. Rey and all the other members of the lab for their help and guidance. She believes that this has been her greatest experience at UCLA, as she has learned about the research process and science in a way that isn’t possible in a classroom setting. She would also like to express her sincere gratitude to the Wasserman family for their generosity and URC for their support and kindness.

 

 

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Ms. Mary Haviland
Mentor:
Funding: Wasserman Scholar
Title:

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Ms. Tuyet Ho
Mentor: Dr. Ren Sun
Funding: Wasserman Scholar
Title:
Characterization of a Regulatory cis-element that Controls the Transcription of a Gammaherpesvirus Latency to Lytic Switch Protein, RTA 

(from left to right): Dr. Ren Sun, Tuyet Ho, Dr. Vaithi Arumugaswami

Tuyet Ho is a 4 th year undergraduate student in the Department of Biochemistry. After getting her bachelor degree from UCLA, she aims to get a PhD and a PharmD degree concurrently. She has been in Dr. Ren Sun’s lab in the Pharmacology Department since Winter 2007. Tuyet would like to thank Dr. Sun, Dr. Arumugaswami, and her scholarship donors for their guidance and supports.

Tuyet’s research focuses on the expression of Replication and Transcription Activator (RTA) of the gamaherpesvirus family. RTA is the key element to regulate the equilibrium between latent and lytic states of MHV-68, a model study of the gamaherpesvirus family. Dr. Sun’s lab has identified a critical cis-element in the RTA promoter region of MHV-68 virus that is essential for completion of the virus lifecycle. Hence, it has been hypothesized that this cis-element is required for transcription of RTA.

To characterize the cis-element, Tuyet will construct a RTA promoter having mutations in the cis-element into a firefly luciferase reporter vector. The luciferase activity will be measured and the critical nucleotides in the cis-elements will be identified. Furthermore, she will observe the effect of the mutation by monitoring the growth and the viral gene expression kinetics of the mutant MHV-68 virus while comparing to that of wild type MHV-68. The information gained from this project would provide more insight into the activation of RTA promoter and the regulation of early lytic genes expression. Elucidating the mechanism of RTA regulation is important to discover new potential therapeutic targets.

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Mr. Kin Wai (Tony) Hung
Mentor: Dr. Utpal Banerjee
Funding: Wasserman Scholar
Title:
Screening for Mutant Phenotypes of AML1-ETO Fusion Protein via P-elements in Drosophila melanogaster

Kin Wai (Tony) Hung is a fourth year student majoring in Biochemistry and Molecular, Cell and Developmental Biology. Currently he is working on a project to screen for mutant phenotypes of a leukemia-causing protein called AML1-ETO using Drosophila melanogaster . Because the role of AML1-ETO in leukemogenesis still remains a mystery, Tony hopes that his research will serve to identify and characterize specific genes that can eventually be important in discovering the cure to acute myeloid leukemia.

During the winter quarter of his freshman year, Tony took his first initiative in research by enrolling into the H.H.M.I. program called U.C.L.A. Undergraduate Research Consortium in Functional Genomics (URCFG). He was fascinated and curious about what he could contribute to research. Under the mentorship of Dr. Utpal Banerjee, he felt that research not only trained him to master laboratory techniques, but to also question and think like a scientist.

This year Tony is applying to medical school, and is very excited to bring what he has learned in research to the future of medicine. Here, Tony would like to thank all his mentors, fellow classmates, URC/CARE, and the Wasserman family for their guidance and generosity. Last but not least, he wants to give his greatest gratitude to his parents for their unconditional presence.

 

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Mr. Nate Jacobs
Mentor: Dr. Michael Fanselow
Funding: Alcott Scholar
Title:
Post-natal destruction of progenitor cells: understanding the role of adult neurogenesis in learning and memory

Nate Jacobs is a fourth year undergraduate majoring in Neuroscience. He is in his third quarter of doing research in the Fanselow lab, where he works with graduate student Jesse Cushman on understanding the functional role of adult neurogenesis in cognition. To investigate the cognitive significance of newly dividing cells in the adult brain, they are using a mouse line which employs the Cre lox P mechanism to remove specific genes necessary for cell division in the central nervous system. Transgenic mice will be able to develop normally prenatally, but after birth will permanently lack neurogenesis. Thus, this model provides an excellent opportunity to investigate the function of adult neurogenesis. The main goal of this research is to understand the behavioral, rather than physiological, deficits of these transgenic mice. Behavioral testing is done in true Fanselow style using a fear conditioning apparatus that is able to test either amygdala dependent or hippocampal dependent learning and memory. Other measures that could be used to probe the transgenic mice’s cognitive abilities include anxiety tests and spatial learning and memory tasks. If there is time before the end of the year, Nate would like to also investigate the effects of exercise on neurogenesis and cognitive ability.

Nate will be graduating this spring, and hopes to work for one year before going to graduate school to pursue a PhD program in neurobiology.

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Profiles of Students