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The Undergraduate Research
Scholars Program2008-2009
Mr. Thai Ha
Ms. Kathleen Hirano
Ms. Tiffany Ho
Ms. Leann K. Hoang
Ms. Anna Hoang
Ms. Jennifer Hranilovich
Mr. Nigel Hsu
Ms. Trish Hubbard
Mr. Majid Husain
Ms. Roxanna Khadem
Ms. Christine Kim
Ms. Jennifer Lau
Ms. Stephanie Lauw
Ms. Yoo Jin Lee
Mr. Suhhee Lee
Mr. Andrew Leung
Mr. Bunkuong Lim
Ms. Sophia Lin
Ms. Jian-Ya Lin
Mr. Peter Lin
Ms. Hui Chia (Angela) LiuMr. Thai Ha
Mentor: Dr. Genhong Cheng
Funding: Boyer Scholar
Title: Herpesviral DNA Ligand Receptor Responsible for Induction of Type-I Interferon
Dr. Genhong Cheng and Thai Ha
Thai Ha is a fourth-year undergraduate student majoring in Molecular, Cell, and Developmental Biology at UCLA. Under the supervision and guidance of Dr. Genhong Cheng and Dr. David Sanchez, he has been conducting research relating to viral immunity since the summer of his third year at UCLA. His short term goal is to find the receptor that binds to a repeated herpes viral DNA-ligand that was previously shown to induce Type-1 Interferon (IFN). The long term goal of his work is to find a way to trigger the body’s innate immune response to herpes viruses through induction of Type-1 Interferon.
Induction of IFN is one way that the human body uses to fight off viral infection. Knowledge about Interferon and its relation to the innate immune system in response to RNA virus infection has been well studied, but it has not been for DNA viruses like the herpes viruses. Currently, we know that RNA viral infection induces Interferon through a cascade of reaction that ultimately leads to the phosphorylation of transcription factors IRF3/7, which in turn induce Interferon genes. Recently, a cytosolic DNA sensor named DNA-dependent activator of IFN-regulatory factors (DAI) is involved in the DNA-mediated activation of innate immune responses. However, a recent review showed that DAI may not be, or is not, the only DNA sensing molecule for the DNA-mediated IFN induction pathway. As a result, the DNA-mediated IFN induction sensor still needs further investigation.
From Dr. Sanchez’s work, he found a 100 bp repeat region of gammaherpesvirus genomic DNA that is sufficient and necessary to induce IFN. This finding pointed out that there is specificity in the induction of IFN by gammaherpesvirus DNA. As a result, Thai seeks to find the receptor that recognizes this 100 bp repeat region DNA that initiates the DNA-mediated IFN induction pathway.
Thai plans on pursuing a career in pharmacy and pharmaceutical science after graduating from UCLA. He would like to thank Mr. Green for the generous scholarship, the URC program, Dr. Genhong Cheng, and Dr. David Sanchez for their support and guidance.
Ms. Kathleen Hirano
Mentor: Dr. Catherine Clarke
Funding: Bonner Scholar
Title: Investigation of metabolic intermediates and gene-enzyme relationships involved in ubiquinone biosynthesis in S. cerevisiae
Kathleen Hirano and Dr. Catherine Clarke
Kathleen is in her fourth year of undergraduate studies, majoring in biochemistry. She began research in Dr. Catherine Clarke’s laboratory in the Department of Chemistry and Biochemistry in January of 2008. She is currently under the mentorship of Dr. Beth Marbois, researching the metabolic pathways of ubiquinone aromatic precursors. She has previously investigated the role of Coq10p under post-doctoral fellow Dr. Susan Morvaridi, specifically studying its role in coenzyme Q localization in relation to membrane fatty acid oxidation.
The coenzyme Q biosynthetic pathway begins with the ligation of a polyisoprenoid tail to the aromatic precursor, 4-hydroxybenzoic acid (pHB). In mammals pHB is obtained from the amino acid tyrosine, while in E. coli it is produced directly from the shikimic acid pathway by UbiC. S. cerevisiae, however, acquires pHB from both pathways but appears to lack the UbiC homolog required to convert chorismic acid to pHB. Instead, recent results suggest that 4-aminobenzoic acid (pABA) serves as a precursor of coenzyme Q. pABA is also derived from chorismic acid through two steps mediated by the gene products of ABZ1 and ABZ2. Additionally, pABA is a precursor in the folic acid synthesis, which, due to its absence in humans, is a common target of drug inhibition in bacterial infections. Current unpublished research has revealed the relationship between coenzyme Q and its precursors through metabolic radio-labeling, HPLC and mass spectrometry. Also, Δabz1 and Δabz2 strains have been previously shown to be dependent on folic acid or pABA supplementation in minimal media by Botet et al. In our lab, Δabz1 and Δabz2 is additionally being assessed for respiratory differences as a possible indicator of coenzyme Q synthesis. Kathleen is currently investigating this aspect of coenzyme Q aromatic precursors, generating multiple gene knockout mutants to isolate specific precursor pathways and analyzing their ability to utilize non-fermentable carbon sources.
Kathleen is grateful for the incredible research experience she has gained, and would like to thank Dr. Clarke and Dr. Marbois and all the members of the Clarke lab for their kindness, generosity and guidance. She would also like to express her gratitude to the Margaret Bonner Estate for their support and for their help in making undergraduate research possible.
Ms. Tiffany Ho
Mentor: Dr. Judith Berliner
Funding: Bonner
Title: Function of small G-proteins in the Action of Ox-PAPC in Human Aortic Endothelial Cells
From left to right: Sangderk Lee (post-doc), Tiffany Ho and Dr. Judith Berliner
Tiffany Ho is a third year Neuroscience major who plans to minor in the field of Gerontology. She has worked in the Berliner lab since Fall of 2007 and greatly appreciates both her primary investigator Dr. Judith Berliner and post-doctorate Sangderk Lee for their hard work and support. After joining this lab, Tiffany has become passionate about research and plans to dedicate her year after graduation towards continuing her project while applying for medical school.
Atherosclerosis is a chronic inflammatory disease that causes major coronary artery diseases such as heart attack and stroke. The Berliner lab has studied the role of oxidized phospholipids in the development of atherosclerosis in the vascular walls. Mimicking minimally-modified low-density lipoprotein (mm-LDL), oxidized 1-palmitoyl-2-arachindonyl-sn-glycerol-3-phosphocholine (Ox-PAPC) activates human aortic endothelial cell (HAEC) and triggers induction of over 1,000 genes including proinflammatory, redox regulating, unfolded protein response, procoagulant, and sterol synthetic genes.
Recently, the role of small G-protiens have shown various pathophysiological regulatory functions in the cells including migration, cytoskeletal rearrangement, and gene transcriptions in the cells. Tiffany plans to further investigate how Ox-PAPC regulates the rearrangement of endothelial adherens junction (AJ), which regulates the permeability of solutes, nutrients, and immune cells through endothelial barrier. Rac1 and cdc42 are two small G-proteins that have been identified to play roles in this phenomenon, and she will examine the relationship of rac1/cdc42 with the activation of VE-cadherin, a key molecule for the formation of adherens junction in the cells.Ms. Leann K. Hoang
Mentor: Dr. James Tidball
Funding: Boyer Scholar
Title: Mitochondrial Dysfunction in Dystrophin-Related Disorders
LeAnn Hoang and Dr. James Tidball
LeAnn Hoang is a fourth-year Physiological Science major. She began her undergraduate research experience at UCI Center for Mitochondrial and Molecular Medicine and Genetics, and then started a joint collaboration with the laboratory of Dr. James Tidball in her junior year. She is studying how the mitochondrion may be a modifying factor in dystrophin-related disorders. Dystrophinopathies are a group of inherited diseases generally characterized by muscular dystrophy, respiratory failure, cardiomyopathy, and early death. Previous studies have found that muscular dystrophy is often associated with muscle fatigue and pathology. Since the mitochondrion is responsible for cellular energy production in muscle and also produces toxic by-products that may result in DNA mutations and increased oxidative stress, mitochondrial dysfunction may play a role in the progression of dystrophinopathies. LeAnn is starting her expression studies using microarrays to analyze the expressions of genes involved in mitochondrial-mediated apoptosis pathways.
LeAnn would like to thank her UCI mentors, Dr. Michael Zaragoza and Dr. Douglas Wallace, and Dr. James Tidball and Armando Villalta at UCLA for their guidance and support. She would also like to thank the URC/CARE Center and Albert C. Boyer estate for supporting her research. She is currently applying to medical school.
Ms. Anna Hoang
Mentor: Dr. Pirouz Kavehpour
Funding: Hilton Scholar
Title: Evolution of the precursor film in front of the moving contact line of a spreading drop
Dr. Pirouz Kavehpour and Anna Hoang
Anna Hoang is a fourth year Mechanical Engineering major at UCLA and has been working since June 2007 as a member of the Complex Fluids and Interfacial Physics Laboratory in the department of Mechanical and Aerospace Engineering. Under the guidance of Dr. Pirouz Kavehpour, she has been studying the evolution of the precursor film in the vicinity of the moving contact line for a spreading drop. For wetting fluids, a microscopic film, which is known as the precursor film, exists at the front of the moving contact line. The structure of this thin film has been studied theoretically, but previous experimental investigations were limited by the resolution of the measurement system (lateral or vertical) required to capture the complete scope of this feature. We studied the evolution of the profile of a spreading droplet near the moving contact line using a total internal reflection fluorescence microscope (TIR-FM). The features of the macroscopic drop (spherical cap), wedge region, and precursor film were investigated within a single experiment. This was made possible by the lateral resolution and dynamic range of our technique. The dynamic characteristics of the precursor films have a good agreement with the available theoretical results. The microscopic dynamics of liquids spreading on solids have many industrial and technical applications such as coating processes, inkjet printing, and cell manipulation. Investigation of the thin precursor film is especially important for developing a fundamental understanding of fluids spreading on solids.
After graduating with a bachelor’s degree, Anna plans on continuing her studies at UCLA as a graduate student. She would like to thank Dr. Kavehpour for his support and guidance as her research mentor.
Ms. Jennifer Hranilovich
Mentor: Dr. Elizabeth Sowell
Funding: Hilton Scholar
Title: Pubertal status predicts medial temporal lobe and cortical gray matter volume in normally developing adolescents
Jennifer Bramen, Jennifer Hranilovich, Elizabeth Sowell
Jennifer Hranilovich is a fourth-year Neuroscience major who transferred to UCLA from Santa Monica College. She began her MRI research during her sophomore year at UCLA, commuting from SMC through an internship program and studying the perception of time with Jennifer Bramen, then a graduate student with Dr. Marc Cohen’s lab. She joined Jennifer at Dr. Elizabeth Sowell’s lab in January of 2008 and will continue there through spring of 2009. During this time she plans to complete an honors thesis under the mentorship of Dr. Sowell and Dr. Bramen.
Dr. Sowell’s lab is focused on the analysis of functional and structural changes in the brain that occur during adolescence, particularly in populations exposed prenatally to meth-amphetamine and alcohol, using MRI and neurobehavioral correlates. Jennifer’s research has been part of a collaboration with a pediatrician’s group that has collected structural MRI of a large sample of healthy boys and girls from a narrow pubertal age range. The study is longitudinal and also includes data on plasma testosterone and estrogen levels. Jennifer has been responsible for the development of a lab protocol for use of a piece of software called FreeSurfer that is capable of automatic identification and segmentation of cortical and subcortical of regions of interest. She has used FreeSurfer to generate volumetric data on medial temporal lobe structures and pre-frontal cortex that allowed the lab to test hypotheses on the effects of puberty and pubertal hormones on the development of these structures.
Jennifer is currently applying to medical schools and plans to attend a program that includes a year of research, in preparation for a career in academic medicine. Jennifer would like to thank the Undergraduate Research Center and the Hilton family for their generosity, and Dr. Elizabeth Sowell, Dr. Jennifer Bramen and the Sowell Lab for their personal and intellectual support of her research.
Mr. Nigel Hsu
Mentor: Dr. Rochelle Crosbie
Funding: Bonner Scholar
Title: Akt Overexpression as a Novel Therapy in Treating Muscular Dystrophy
Chris Ko, Nigel Hsu, Elizabeth Canales, Jamie Marshall, Jenna Wilson, Michelle Kim, and Dr. Rachelle Crosbie
Nigel Hsu is a fourth year student majoring in Physiological Science. He has been a member of Dr. Crosbie’s muscular dystrophy lab since December 2007 under the mentorship of graduate students Michelle Kim, Chris Ko, and Jamie Marshall. The Crosbie lab focuses on discovering novel therapeutic treatments to alleviate dystrophic pathology utilizing mdx mice models.
There are several forms of muscular dystrophy. The most prevalent form, Duchenne Muscular Dystrophy, is caused by mutations in the dystrophin gene. This results in not only a loss of the dystrophin protein, but the entire dystrophin-glycoprotein complex (DGC) as well which leads to sarcolemmal instability and progressive muscle wasting. Recently, Nigel and his group published a paper in Human Molecular Genetics, titled “Myogenic Akt signaling upregulates the utrophin-glycoprotein complex and promotes sarcolemma stability in muscular dystrophy” that shows by increasing Akt levels in dystrophic mice models, there is an increased expression of utrophin, a functional homologue of dystrophin, as well as the other proteins in the utrophin-glycoprotein complex (UGC). The UGC functionally replaces the DGC and rescues several aspects of dystrophic pathology. With these findings, Nigel is currently exploring localized treatment of mdx mice quadriceps with adenovirus vectors loaded with caAkt and dnAkt.
Nigel plans on attending medical school in the near future while still continuing with research work. He would like to thank Dr. Crosbie for giving him the opportunity to contribute to this exciting research and the Bonner estate for their generous support.
Ms. Trish Hubbard
Mentor: Dr. Jerome Zack
Funding: Wasserman Scholar
Title: Determining efficacy of antiretroviral drugs in primary macrophages
Trish Hubbard and Dr. Jerome Zack
Trish Hubbard is a fourth-year undergraduate student working towards a B.S. in Anthropology with a minor in Mexican Studies at UCLA. Since her sophomore year she has been working in the Zack lab under the guidance of Matthew D. Marsden, PhD in the Department of Microbiology, Immunology, and Molecular Genetics. Her primary objective is to establish the effectiveness of various antiretroviral drugs in primary macrophages.
Several antiretroviral agents have not been comprehensively tested in for efficacy in primary macrophages. It is important to know how efficiently these drugs prevent infection of macrophages because these cells are a significant reservoir of HIV in vivo and play an important role in viral persistence and pathogenesis. Trish has been using plasmid clones and non-replication competent HIV-based vectors to address this question. She has constructed HIV-vectors and virus, and will isolate primary monocytes from peripheral blood of healthy individuals for differentiation in vitro. Vectors will then be used to establish concentrations of antiretroviral drugs that are effective at inhibiting single-round HIV infection of primary macrophages. Furthermore, the study will determine the post-infection therapeutic window in which addition of these drugs is still effective at suppressing infection.
Trish Hubbard is planning to attend medical school in her near future, and hopes to pursue a career serving the Latino community. She would like to thank Matthew D. Marsden, PhD and Jerome A. Zack, PhD for their patience, their guidance, and for the opportunity to conduct research. She would also like to thank the Wasserman family for their interest in her success.
Mr. Majid Husain
Mentor: Dr. Alvaro Sagasti
Funding: Wasserman Scholar
Title: A chemical screen to identify new pathways involved in trigeminal axon arbor development in Zebrafish
Dr. Alvaro Sagasti and Majid Husain
Majid Husain is a fourth year undergraduate majoring in psychobiology. Post graduation he plans to purse a career in medicine. Majid has been working in Dr. Alvaro Sagasti’s laboratory for the past 3 years. He has been involved in various projects dealing with the development of the trigeminal sensory neurons in zebrafish.
The trigeminal neurons are responsible for sensing pain, touch & temperature. Previous studies have shown that territories of peripheral axons of trigeminal neurons are limited by repulsion between these axons during development. Growing trigeminal arbors repel each other at the top of the head causing them all to stop growing roughly at the midline. The focus of Majid’s study is to search for factors that mediate these repulsive interactions. He will be using a library of kinase inhibiting drugs with known targets to test their effects on the trigeminal arbors. To visualize the axons, a homozygous transgenic line that expresses KikGR, a photo convertible fluorescent protein, in the trigeminal neurons, will be used. The photo convertibility of the KikGR protein from green to red using a UV laser allows visualization of the left and right trigeminal ganglia and their growing peripheral axons in different colors. Any unusual growth pattern can then be attributed to the effect of that particular drug.
Majid would like to thank Dr. Alvaro Sagasti as well as all the members of the lab for their constant help, support and mentorship. Majid would also like to thank the Wassermann Family for their generous donation.
Ms. Roxanna Khadem Mentor: Dr. Ann Hirsch Funding: Sparks Scholar Title: Burkholderia tuberum : the beta rhizobium that nodulates legumesDr. Ann Hirsch and Roxanna Khadem
Roxanna Khadem is a fourth-year undergraduate student majoring in Molecular, Cell, and Developmental Biology (MCDB). After taking MCDB 120 with Dr. Hirsch in the fall of 2007, she became more interested in plant biology. She has been working Dr. Hirsch’s laboratory since winter of 2008.
Members of the Hirsch lab study the interactions between nitrogen-fixing bacteria and legumes. Roxanna is currently studying different strains of the bacterium Burkholderia tuberum that have been mutagenized with the pUT-gfp plasmid. She will be performing various assays to determine the location of the gfp insertions and the number of insertions. Specifically, she will be studying the motility, swarming activity, exopolysaccharide production and biofilm formation of the mutants. She will also test whether these mutants and the wildtype bacteria are able to nodulate the legume siratro and fix nitrogen. If the mutants effectively nodulate siratro, the gfp marker can be used as a means of tracking them once they are inside the plant. Roxanna hopes to better understand the symbioses between nitrogen-fixing bacteria and legumes with the hope that this knowledge can be used to grow crops, including those used for biofuels, using less chemical fertilizers, whose production requires energy from fossil fuels.
Roxanna is currently applying to dentistry school. She would like to thank Dr. Hirsch, everyone in the Hirsch lab, the URC/CARE, and Sparks for supporting her interest in plant biology.
Ms. Christine Kim
Mentor: Dr. Anna Taylor
Funding: Hilton Scholar
Title: Sex Differences in Ethanol-Induced Hypothermia in Ethanol-Naïve and Ethanol-Dependent/Withdrawn Rats // Lasting neuro-endocrine-immune effects of traumatic brain injury (TBI) in rats
Christine Kim and Dr. Anna Taylor
Christine Kim is a fourth year undergraduate student majoring in Molecular, Cell, and Developmental Biology (MCDB) at UCLA. She has been conducting research in Dr. Anna N. Taylor’s lab since her second year in the Department of Neurobiology. Christine currently works on the study relating to the thermoregulatory responses of alcoholism and the possible causes of these differences between male and female.
There are various well known studies that involve different behavioral responses between male and female to ethanol (EtOH) dependence and withdrawal; however, different effects on physiological adaptations, such as thermoregulation, between the two genders currently lack extensive study. Since progesterone derived neurosteroids have the ability of enhancing the actions of GABA at receptors, they may alter aspects of sexual and alcohol related behaviors. Christine’s study involves the blocking of the derivative pathways of progesterone to inhibit the activity of 5α-reductase in order to further analyze and observe its effects on hypothermic responses to acute alcohol injections to female and male rats. She is aiming to understand and discover the major cause of sex differences in hypothermic responses to alcohol, such as endogenous differences between male and female.
Christine is also involved with the study in lasting neuro-endocrine-immune effects of traumatic brain injury (TBI) in rats, which is conducted in parallel to the ethanol study. She hopes to delve into the possible long term effects of traumatic brain injury in the neuro-endocrine system to the behaviors of rats, hoping to relate and apply our studies to TBI in humans.
Christine is thankful for the continuous guidance and support she has received from Dr. Taylor and Delia Tio. She also would like to thank Diane & Henry Hilton and URC/CARE for their generous support.
Ms. Jennifer Lau
Mentor: Dr. Hong Wu
Funding: Boyer Scholar
Title: Investigation of Novel Pathways Regulated by PTEN in Murine Embryonic Stem Cells Stress Defense(from left to right): Dr. Jing Jiao, Jennifer Lau and Dr. Hong Wu
Jennifer Lau is a fourth-year Molecular, Cell and Developmental Biology major with a minor in Biomedical Research. Since Spring 2007, Jennifer has been conducting research at Dr. Hong Wu’s lab in the Department of Molecular and Medical Pharmacology, David Geffen School of Medicine under the guidance and supervision of Dr. Jing Jiao, a post doc fellow at Dr. Hong Wu’s lab.
Her ongoing research focuses on identifying novel pathways regulated by PTEN in murine embryonic stem cells stress defense. Oxygen-free radicals, known as reactive oxygen species (ROS) are constantly produced by living organism as by-products of mitochondria-catalyzed electron transport reactions and other mechanisms in living organisms. H igh level of ROS production affects cellular functions via damaging nucleic acids, cell structures, proteins and lipids . Such oxidative damage has been shown as a critical factor in aging, mutagenesis and cancer progression . Studies have reported that murine embryonic stem cells (mESC) have a highly proficient antioxidant defense against ROS than that of differentiated murine cells. PTEN ( phosphatase and tensin homologue deleted on chromosome 10) is a frequently mutated tumor suppressor gene complicated in various human tumors, including prostate, endometrial and breast cancers. A recent study has also reported that PTEN deletion in mouse embryonic fibroblasts (MEFs) leads to deregulated expression of antioxidants and decreased antioxidant defense ability, suggesting an essential role of PTEN in maintaining a normal redox state for MEFs against oxidative damages. Oxidative stress on tissues and cells has been widely recognized as a key factor effecting embryonic development . However, the effects of PTEN deletion on embryonic stem cells , in the context of oxidative stress, have not been thoroughly studied to date. Taken together, Jennifer is currently conducting her honor thesis under mentorship of Dr. Jing Jiao to study the role of PTEN in embryonic stem cells stress defense using PTEN wild type and PTEN null ES cells established by previous lab members.
Results derived from this study will provide us molecular insight as to how PTEN deletion might play a role in embryonic stem cell stress defense, which ultimately provide us better understanding and characterization of PTEN in ES cells function and carcinogenesis.
Jennifer plans on continuing research in the future with the eventual goal of attending medical school. Jennifer is extremely grateful to her mentor, Dr. Hong Wu and her post doc Dr. Jiao Jiao, for their unlimited patience and support and for giving her such an invaluable opportunity to contribute to the lab. She would like to thank Boyer for its generous support as well as the rest of the Wu lab for their guidance and support. She would also like to express her gratitude to the Undergraduate Research Center for extending this exciting opportunity.
Ms. Stephanie Lauw
Mentor: Dr. Luisa Iruela-Arispe
Funding: Van Trees Scholar
Title: The Role of ADAMTS-1 in Cardiovascular Development and Neurogenesis
(From left to right: Dr. Antoni X. Torres-Collado, Stephanie Lauw, Dr. Luisa Iruela-Arispe)
Stephanie Lauw is a 4 th year Molecular, Cell, and Developmental Biology major with a minor in Biomedical Research. She has been working under the direction of Dr. Luisa Iruela-Arispe since the summer of 2007. She is currently studying the effect of the genetic inactivation of A Disintegrin And Metalloprotease with Thromsbospondin Repeat-1 (adamts-1) on the cardiovascular and neuronal development of mouse embryos.
Adamts-1 is a protease secreted into the extracellular matrix (ECM) and synthesized by a subset of epithelial cells in the kidney, pancreas, exocrine glands, lung, and hair follicles. In the adult mouse, genetic inactivation of adamts-1 results in pathologies in the kidneys, adipose tissue, and the female reproductive system. In the embryo, genetic inactivation of adamts-1 results in a 40% prepartum mortality rate at embryonic day 9.5 which cannot be attributed to the kidney failure that causes adult mortality. The purpose of Stephanie’s studies is to determine the cause of the embryonic lethality by assessing adamts-1 null embryos at the cardiovascular, hematopoetic, and neuronal level.
After graduating, Stephanie hopes to attend medical school. She would like to thank the scholarship for its donation to enhance her experience at UCLA, and Dr. Arispe and Dr. Torres-Collado for their guidance and support.
Ms. Yoo Jin Lee
Mentor: Dr. Karen Lyons
Funding: Alcott Scholar
Title: Molecular mechanism behind ALK5 receptor signal transduction
Dr. Karen Lyons and Yoo Jin Lee
YooJin Lee is a fourth-year undergraduate Molecular, Cell, Developmental, Biology (MCDB) major at UCLA. She has been an Undergraduate Research Student Program student in Dr. Karen Lyon’s lab since Fall 2007. Under the supervision of Dr. Buer Song, she is exploring the molecular mechanism behind TGF-β signal transduction in vivo.
TGF-β is involved in cellular transformation and regulates many various cellular functions such as cell replication, differentiation, cell cycle, and cellular migration, and developments such as bone formation, angoiogenesis, and haematopoiesis. Also, TGF-β superfamily growth hormones are very important molecules in the development and maintenance of articular cartilage; however, roles of TGF-β have not been clearly understood. TGF-β receptor subdivides into type I and type II, and binding of TGF-β to its receptor starts cascade of signal transduction by molecules called Smad. YooJin will be focusing on investigating the underlying mechanism of ALK5, TGF-β type I, receptor activation and identifying intracellular TGF-β signaling molecules such as Smad 1, 2, 3, 5, 8, and other MAPK signaling patyway compoenets that are involved.
YooJin thanks her mentors Dr. Karen Lyons and Dr. Buer Song for a chance to research in their lab. She also thanks Dr. Cramer for the Undergraduate Research Scholars Program and Mr. Webster for his generosity.
Mr. Suhhee (Rachel) Lee
Mentor: Dr. Reuben Kim
Funding: Wasserman Scholar
Title: The Regulation of p53 during Cellular Senescence and Organismal Aging
Rachel Lee and Dr. Reuben Kim
Rachel Lee is a fourth-year undergraduate student majoring in Molecular, Cell and Developmental Biology. She first began working in a research laboratory during her sophomore year. Since Fall 2007, she has been a member of Dr. Reuben Kim’s laboratory, which is under the UCLA School of Dentistry, and has been involved in studying the role of p53 in the cellular senescence.
The long-term goal of Dr. Reuben Kim’s laboratory is to study the role of p53 in the cellular senescence of normal human epithelium including keratinocytes, and its role in age-associated diseases such as cancers. P53 is a well-known tumor suppressor gene that is usually inactive in normal cells. Upon genotoxic stresses, p53 becomes activated, and induces cell cycle arrest or apoptosis. In the field of senescence, the role of p53 is extensively studied using normal human fibroblasts. In normal human fibroblasts, senescence is accompanied by either increased expression or transactivational activity of p53. Unlike the human normal fibroblast, however, human normal keratinocytes have shown to exhibit a decreased p53 protein expression during senescence. As a consequence, it has been suggested that the loss of UV-induced apoptosis in senescent keratinocytes is associated with the loss of p53 expression. Because the loss of p53 is physiologically significant, especially in older individuals who are more prone to have age-associated diseases including cancers, the role of p53 in senescence and aging processes warrants closer examination.
The regulation of p53 occurs at the transcriptional level by numerous genotoxic stresses, but it also occurs heavily at the post-transcriptional level through ubiquitin-proteasomal degradation pathway. Important regulators of p53 stability and degradation are MDM2 and MDM4. Low expression of p53 is primarily attributed to the MDM4-mediated ubiquitinlyation and MDM4-mediated transactivation domain occlusion of p53. Therefore, we hypothesize that the loss of p53 protein expression level during senescence is altered expression patterns of p53 regulators, MDM2 and MDM4. To test this hypothesis, we will serially subculture NHOK and screen for the expression patterns of p53, MDM2, and MDMX. B-Actin will be also probed as a loading control. To validate the findings, I will perform this experiment in three different strains of NHOK which are derived from normal oral epithelium of three independent donors. We anticipate that the expression of p53 and MDM2/MDM4 are inversely correlated. The result we will obtain from the current study will help elucidating the mechanism by which p53 losses its expression during senescence.
After graduating from UCLA, Rachel plans on pursuing a career in dentistry. Rachel would like to thank the Wasserman family for their generous scholarship and Dr. Kim for his guidance and for giving her the opportunity to contribute to his research laboratory.
Mr. Andrew Leung
Mentor: Dr. Grace Griesbachl
Funding: Bonner Scholar
Title: Assessing the effect of exercise on post-traumatic brain injury recovery in rats
Dr. Grace Griesbach and Andrew Leung
Andrew is a fourth year Neuroscience major and Political Science minor. After taking the core classes for his major, Andrew became fascinated with the neuronal world and began research under the tutelage of Dr. Grace Griesbach in October 2008.
The project he will be assisting on attempts to ascertain the effects of exercise on traumatic brain injuries in rats. Brain trauma is a significant cause of injury and disability, and its replication in rats provides a useful research model. Andrew will assist in conducting various behavioral tests such as the Morris water maze or novel-object recognition tasks for overall function and various immunoassays for molecular involvement. These molecules include cyclic AMP response element binding protein (CREB) and synapsin I, which are downstream to brain-derived neurotrophic factor (BDNF). Although BDNF is found throughout the brain, it is mostly localized in the hippocampus which emphasizes its role in learning and memory, a characteristic key to brain trauma recovery. Phosphorylation of synapsin has been linked to neurotransmitter release. Knowing the relative amounts of these molecules lends information regarding which processes in the molecular pathway are most crucial for recovery of function. He will also investigate the role of the stress response in BDNF and function, as well as their overall effect on synaptic plasticity, which is critical for recovery.
Andrew would like to thank the Undergraduate Research Center and Dr. Griesbach for her guidance and the opportunity to be an active participant in the field of neuroscience. He also thanks Bonner and its scholarship committee for its generosity and financial support.
Mr. Bunkuong Lim
Mentor: Dr. Steve Jacobsen
Funding: Van Trees Scholar
Title: Identifying functional histone demethylase protein in the plant Arabidopsis thaliana
Dr. Guillaume Moissiard, Bunkuong Lim, Dr. Steve Jacobsen
Bunkuong Lim is a fourth year Biology major. He has been conducting research under the guidance of Dr. Guillaume Moissiard and Dr. Steve Jacobsen in the department of Molecular, Cell and Developmental Biology for almost a year. His project involves identifying functional histone demethylase proteins in the plant Arabidopsis. It is commonly known that transcriptionally silenced genes are observed to have methylated lysine number 9 on the third histone tail (H3K9), H3K27 and H4K20; whereas transcriptionally active genes are observed to have methylated H3K4, H3K36 and H3K79. Therefore depending on their methylation marks, some genes will get expressed while others get suppressed. Histone tail demethylase genes encode Jumonji (JMJ) proteins. Currently, a few genes that are thought to belong to the JMJ family are being studied. Each of them is overexpressed in transgenic plants and its global methylation marks are then measured and compared to the wildtype’s mark. It is expected that when a JMJ gene is overexpressed, there should be an increase and decrease in specific methylation mark.
Bunkuong would like to thank Dr. Guillaume Moissiard and Dr. Steve Jacobsen for their guidance. Also, he would like to thank the Knapp family for their generous support.
Ms. Sophia Lin
Mentor: Dr. Daniel Kamei
Funding: Bonner Scholar
Title: siRNA delivery using polypeptide co-polymer vesicles
Sophia Lin and Dr. Daniel Kamei
Sophia Lin is a third year undergraduate student majoring in chemical and biomolecular engineering. She has been working in Dr. Kamei’s laboratory in the Department of Bioengineering since April 2008 and has been examining the ability of vesicles to act as a drug delivery vehicle.
Vesicles are composed of a range of amphiphiles that self assemble based on their hydrophobic and hydrophilic fraction. Depending on the insertion method, these vesicles are able to encapsulate the proposed substance and release their contents in the cytoplasm upon stimulation. Because of its biomimetic nature, vesicle based delivery shows promise as a therapeutic application.
The delivery of siRNA into cells using these co-polymer vesicles is going to be examined and the gene knockdown will be compared to that of commercial delivery agents. In addition to that, the project involves quantifying vesicle uptake efficiency, protein expression, and cell viability.
Sophia would like to thank Dr. Kamei and the other members of the Kamei lab for their support and guidance as well as the Bonner estate for their generosity.
Ms. Jian-Ya Lin
Mentor: Dr. Benhur Lee
Funding: Van Trees Scholar
Title: Mechanism of Gal-1 Involvement in Enhancement of HIV Infection
Dr. Patrick Hong, Jian-ya Lin and Dr. Benhur Lee
Jian-ya Lin is a fourth year Microbiology, Immunology, and Molecular Genetics major. She is continuing her second year of research at the Lee lab under the guidance of Dr. Benhur Lee and Dr. Patrick Hong. Currently her research involves galectin-1, a member of the highly conserved β-galactoside binding lectin family, and its involvement in the relocation of CD43 and CD45 on dendritic cells (DCs). Galectin-1, expressed by various cell types such as T cells, dendritic cells, etc., have been reported to enhance HIV-1 infection via cells to pathogens interaction due to its homodimeric nature. CD43 and CD45 are cell surface receptors located on MDDCs (monocyte-derive DCs) which can mask CD4 and coreceptors (CCR5 and CXCR4), main receptors for HIV-1 entry. Therefore, Jian-ya wants to find out if galectin-1 has the ability to relocate CD45 and CD43 exposing CD4 and coreceptors and thus allowing HIV-1 infection. Furthermore, galectin-1 treated MDDCs will be incubated with green fluorescent HIV-1 to observe the location of the virus in respect to CD43 and CD45 via confocal microscopy.
Jian-ya would like to express her gratitude to Dr. Benhur Lee for the opportunity to research in the Lee lab, Dr. Patrick Hong for his patience and continuous support, and the Van Tree family for their generous donations. She plans on attending pharmacy school and becoming more involved in pharmaceutical research after graduating from UCLA.
Mr. Peter Lin
Mentor: Dr. Kelsey Martin
Funding: Wasserman Scholar
Title: Nuclear translocation of Transducer of Regulated CREB Activity (TORC) protein in hippocampal neurons
Peter Lin and Dr. Kelsey Martin
Peter Lin is a third year majoring in Neuroscience and minoring in Biomedical Research. He has been in the Kelsey Martin lab under the mentorship of Dr. Toh Hean Ch'ng.
The lab is interested in s tudying the molecular mechanisms of synapse-to-nucleus signaling during long-term memory formation. In particular, the lab focuses on identifying protein cargoes that translocate to the nucleus via the classical nuclear import pathway during synaptic stimulation which results in long-term memory formation. One of these possible cargoes includes TORC protein (transducer of regulated CREB activity protein), the subject of his project. Although TORCs have important roles in several types of cells, TORCs have been found to be necessary for LTP (long-term potentiation) in hippocampal neurons, suggesting that they have a vital role in the formation of memories. His project involves characterizing the pathway by which these TORC proteins are activated, using a combination of pharmacological treatments and fluorescent imaging of rat hippocampal neurons.
Peter plans to apply to a graduate research program. He would like to thank Drs. Toh Hean Ch'ng, Kelsey Martin and Ira Clark and the Wasserman family for all of their help.
Ms. Hui Chia (Angela) Liu
Mentor: Dr. Paul Mischel
Funding: Wasserman Scholar
Title: Therapeutic Implications of Dep-1 as Mediator of Crosstalk between Receptor Tyrosine Kinases and Key Molecular Target of Resistance and Adaptation in Glioblastoma
David Nathanson, Angela Liu and Dr. Paul Mischel
Angela Liu is currently a fourth year Neuroscience major. She has joined Dr. Paul Mischel’s research lab in the Pathology and Laboratory Science Department in the David Geffin School of Medicine since Fall quarter of my sophomore year, 2005.
The research of Mischel lab focuses on the translational approach to the treatment and diagnosis of glioblastoma, the most invasive primary adult brain tumor. In an effort to elucidate the therapeutically exploitable molecular target in glioblastoma, ongoing projects delve into signaling transduction feedback mechanism and crosstalk that confer resistance to traditional pharmacological treatments. Moreover, microfluidic nanotechnology has also been developed as a potential clinical diagnostic tool to achieve single-cell analysis and parcel highly heterogeneous cancer populations, providing crucial information in terms of selection and adaptation of tumor cells that dictate patient treatment response. The work from the Mischel lab has contributed tremendous breakthroughs to the medical paradigm of combinational and personalized medicine.
Her ongoing research project focuses on the density-enhanced phosphatase (DEP-1), a receptor-type protein tyrosine phosphatase. Previous research has indicated interaction between Dep-1 and many other receptor tyrosine kinases (RTKs) amplified in glioblastoma, including PDGFR (platelet-derived growth factor receptor), Met, and VEGFR (vascular endothelial growth factor receptor). RTKs are frequently up-regulated to sustain essential signals of cell survival and nutrient metabolism required by proliferating tumor cells. This molecule came to our attention based on the findings of co-activations of multiple RTKs that indicate re-wiring and the ability of cancer populations to adapt to molecular therapy against single RTKs. We suspect that Dep-1 may play an important mediator role of the crosstalk signal between various RTKs in glioblastoma. To approach this hypothesis, she will be using immunoprecipitation technique to screen for RTKs that might associate with Dep-1 in established glioblastoma cell lines T98 and Ln229. Furthermore, SiRNA knockdown and overexpression Dep-1 models will be used for biochemistry analysis in order to delineate the functional phenotype of these associations. The project aims to understand the molecular mechanism of Dep-1 that may enable resistance and adaptation of cancer cells.
Angela is extremely grateful for the opportunities and guidance provided by Dr. Mischel and the continual support from my graduate student mentor, David Nathanson. She feels that she could not have been more fortunate to have such experience of translational clinical research and to work toward such an important cause of realizing personalized medicine. Angel would also like to give special thanks for the Wasserman family for their financial support for undergraduate research and the Undergraduate Research Center for their coordination of this program.
