Labs interested in BS/MS Students

Overview

The Komiyama lab at the Center for Neural Circuits and Behavior has one position available for a BS/MS student who will perform research on neural circuit functions in behavior. The student will work closely with a postdoctoral fellow and apply the techniques of brain histology, immunostaining, imaging, mouse behavior training, etc.

Requirements

Must be willing to work with mice. Lab coursework preferred. Minimum 12 hrs/wk during the BS portion of the program.

Contact Information

Takaki Komiyama

Department of Neuroscience

tkomiyama@ucsd.edu

Overview

Our research focuses on obesity, gestational diabetes and intrauterine metabolism.

Requirements

• Motivated students with a desire to pursue a medical or biomedical research career

Contact Information

Jianhua Shao

Pediatrics

jishao@ucsd.edu

Overview

Our lab is interested in understanding the signaling pathways that regulate mitochondrial function and turnover in cardiac myocytes. Defects in these pathways contribute to loss of cardiac myocytes and development of heart failure.  Cardiac myocytes are highly active cells that require large amounts of energy supplied by mitochondrial oxidative phosphorylation. Since mitochondria are critical to myocyte function, it is not surprising that there is a strong link between mitochondrial dysfunction and cardiovascular disease. Defective mitochondria can also activate of cell death pathways which can lead to loss of cardiac myocytes and reduced ability to sustain contractile function. This ultimately contributes to the development of heart failure. Therefore, the ability of the cell to overcome mitochondrial damage requires removal of the impaired mitochondria via autophagy.Autophagy is an evolutionarily conserved process involved in the degradation of long-lived proteins and organelles.

Project #1: The E3 ubiquitin ligase Parkin plays an important role in labeling dysfunctional mitochondria for degradation in cells. Parkin is normally localized in the cytosol but rapidly translocates to damaged mitochondria to promote their degradation by ubiquitinating proteins in the outer mitochondrial membrane. The ubiquitin serves as a signal for autophagic degradation. This project will explore the mechanisms underlying Parkin-mediated clearance of mitochondria in cells.

Project #2: MCL-1 is an anti-apoptotic Bcl-2 protein which is expressed at high levels in the heart compared to other anti-apoptotic Bcl-2 proteins. However, very little is known with respect to how MCL-1 regulates cell survival in cardiac myocytes. We have discovered that cardiac specific deletion of MCL-1 lead to mitochondrial dysfunction and rapid development of heart failure, suggesting that MCL-1 is critical for myocyte survival. We have found that one function of MCL-1 is to promote degradation of damaged mitochondria. In this project, the student will investigate the molecular mechanisms by which MCL-1 regulates mitochondrial clearance in cells.

Contact Information

Asa Gustafsson

Skaggs School of Pharmacy and Pharmaceutical Sciences

abgustafsson@ucsd.edu

Overview

Project related to circadian rhythms in brain cells, and relation to depression-like behavior in mice.

Requirements

• Some lab experience who has taken the basic undergrad Circadian Biology course

Contact Information

David K. Welsh

Department of Psychiatry

dkwelsh@ucsd.edu

Overview

Research opportunities are available in a multidisciplinary laboratory studying fundamental questions in Immunobiology and RNA biology. Ongoing projects include: (1) Bioinformatics and systems medicine using HT genome sequencing of blood cells from cancer and AIDS patients. (2) CRISPR-Cas9 applications in immune system engineering. (3) Developing new approaches for cancer immunotherapies.

Additional Info: Under supervision of a postdoctoral fellow or a staff scientist, you will be exposed to: bioinformatics analyses of large genomics data sets, culturing and differentiation of stem cells, drug discovery, viral transduction, RNA and DNA isolation, PCR and gel electrophoresis, transfection, western blot, in vivo and in vitro cancer models, and lab maintenance. For additional information about projects and publications, see http://biomedsci-db.ucsd.edu/faculty_detail?f=249

Requirements

• Must have a strong desire and commitment to perform scientific research in human disease mechanisms
• Must have an understanding of biochemistry, bioinformatics, chemistry, cell biology, or molecular biology
• Prior lab experience is a plus

Contact Information

Tariq Rana

Pediatrics and Genetics

trana@ucsd.edu

Please submit a resume, cover letter, and unofficial transcript to trana@ucsd.edu.

Overview

Astrocytes are support cells in the brain. Although astrocytes harbor pathological hyperphosphorylated tau and neurofibrillary tangles, hallmarks in neurodegenerative diseases, how they contribute to disease is not clear. This project is to investigate tau phosphorylation and tau splicing in human astrocytes. We have preliminary results, which show that tau phosphorylation and tau splicing in astrocytes are significantly different from neurons, suggesting that the mechanisms regulating tau protein modification is different in astrocytes than neurons. These important questions will be answered by comparing human astrocytes and neurons derived from human induced pluripotent stem cells. The student will learn to cultures human astrocytes and neurons, quantitative PCR, immunofluorescent staining, and Western blot.

Contact Information

Shauna Yuan

Department of Neuroscience

shyuan@ucsd.edu

Overview

Our research is focused on understanding the mechanisms by which experience controls the development of the brain. The lab addresses this fundamental neuroscience question by examining the development of the visual system in Xenopus tadpoles, which is well known for its experience-dependent plasticity. Using in vivo imaging, electrophysiology, behavioral assays, and manipulation of gene expression, we have discovered that neuronal activity regulates the development of the visual system through a variety of mechanisms, including changes in neuronal structure, synaptic strength, synaptogenesis, and gene expression.

 The tadpole visual system is highly dynamic and We have shown that animals can recover visually-guided behaviors after brain injury. We are investigating the response to injury.

We have 3 types of projects. 1: students will use the tadpole system to study mechanisms controlling recovery from brain injury. Students will be exposed to methods including whole-brain electroporation, in vivo imaging, immunofluorescence, molecular biology, biochemistry, tadpole husbandry, and general lab techniques. They will learn animal behavior assays and analysis as well. 2: students will participate in a project on computational bioinformatic analysis of RNA Seq data from Xenopus brain tissue. 3: students will participate in a project investigating visual response properties using electrophysiological or imaging methods and quantitative data analysis. Students will be part of a dynamic group of scientists seeking to understand the fundamental aspects of cellular neuroscience using modern molecular techniques and state of the art technology.

Contact Information

Hollis Cline

Department of Neuroscience

cline@scripps.edu

Overview

Potential projects are:

1. In vitro transcription studies on synthetic DNA
2. Structure and function studies of transcription-coupled repair
3. Structure and function studies of chromatin remodeling

Contact Information

Dong Wang

Skaggs School of Pharmacy and Pharmaceutical Sciences

dongwang@ucsd.edu

Overview

Contact Information

Prashant Mali

Bioengineering

pmali@ucsd.edu

Overview

We study protein tyrosine phosphatases, enzymes that play an important role in signal transduction and are critical for numerous cellular processes in health and disease. We have projects available to biochemically and biophysically characterize protein tyrosine phosphatases that are involved in the immune response and play a role in autoimmunity and cancer immunosurveillance.

Requirements

• Previous laboratory and rodent handling experience is highly advantageous

Contact Information

Overview

Information about the Huilin Zhou Lab Projects can be found at: https://www.huilinzhoulab.org/

Requirements

• We prefer interested students that meet the minimum BS/MS GPA requirements

Contact Information

Huilin Zhou

Department of Cellular and Molecular Medicine

huzhou@ucsd.edu

Overview

The Big Picture: A central question in developmental biology is how cells in an embryo become different from one another. Many years of research have shown cellular diversity arises as a consequence of cells interacting with their immediate environment and receiving instructive signals from neighboring cells and the extracellular matrix. Like the developing embryo, human pluripotent stem cells (hPSC) maintained in the laboratory communicate with one another using signaling molecules and thereby either maintain their pluripotent state or assume new properties. Recreating the cellular microenvironments and reiterating the developmental signaling events by controlling the dosage, timing, and combinations of developmental signaling molecules is of critical importance in establishing protocols for reproducible generation, expansion and lineage specific differentiation of hPSCs.

What We Study: In my laboratory we study a major class of signaling proteins encoded by the WNT gene family, which exerts potent effects on stem and progenitor cells. Despite a vast body of research on the role and mode of action of WNTs in developmental biology, how these signaling proteins control cell fate choices of hPSC is poorly understood.  A long-term goal of the lab is to develop methods and protocols to specifically manipulate stem cell fate with WNT proteins, thereby providing the means to derive and isolate mature cell populations. 

The Lab Environment: The Willert laboratory is located in the Sanford Consortium for Regenerative Medicine (SCRM), where over 25 PIs with stem cell interest have established their research programs. At present, 8 full time scientists work in the Willert lab: one post-doc, two Ph.D. students, two Masters student, and 3 lab technicians. In addition, two undergraduate students work in the lab on a part-time basis. We have weekly lab meetings at which individual lab members present their research progress and future plans. SCRM offers a highly interactive environment with several scientific seminar series.

Potential Projects:

1. Protein engineering. WNT proteins are potent stem cell factors that, depending on cellular context, promote self-renewal or differentiation. However, WNT proteins are difficult to isolate as bioactive molecules, which has limited their usefulness in cell and tissue engineering. We have developed approaches to overcome these obstacles by engineering novel WNT-like proteins. A student working on this project will learn how to purify proteins and test activities on hPSCs.
2. WNT signaling in blood development. Blood stem cells are widely used in the clinic to treat a variety of incurable diseases, however, supplies of patient-matched blood stem cells are limited. Developing protocols to generate blood stem cells from hPSCs would be revolutionary in regenerative medicine. Using zebrafish as a model system we found that a specific Wnt gene is required for proper blood stem cell development (Grainger et al. Cell Reports, 2016). Furthermore, we found that this WNT requirement is conserved in humans (in press). A student working on this project will have the opportunity to work with human pluripotent stem cells and differentiate them towards blood lineages.
3. The role of FZD7-WNT signaling in stem cells and cancer. We have found that the WNT receptor FZD7 is required for maintenance of hPSCs in a pluripotent state (Fernandez et al. PNAS, 2014). In the course of these studies, we developed an antibody to FZD7, which inhibits WNT signaling through this receptor. FZD7 has also been found to have important roles in cancer, and our antibody represents a unique opportunity to block cancer growth. An intern working on this project will have the opportunity to work with human pluripotent stem cells and human cancer cells and test the hypothesis that disruption of WNT-FZD7 signaling blocks stem and cancer cell growth.

Requirements

• The only requirements I have is that a student can commit a minimum of 1 year (preferably longer) to my lab and that they are interested in and excited by research.

Contact Information

Karl Willert

Department of Cellular and Molecular Medicine

kwillert@ucsd.edu

Overview

Diabetes is a complex disease characterized by the inability to control blood glucose levels. The hormone insulin is essential for blood glucose regulation, and insufficient insulin production underlies both type 1 and type 2 diabetes. Insulin is secreted into the bloodstream by pancreatic beta cells. In diabetes, beta cells fail to produce sufficient insulin due to either their destruction by the immune system (in type 1 diabetes) or an excessive demand for insulin exceeding beta cell functional capacity (in type 2 diabetes). Therefore, strategies to augment insulin production by improving beta cell function or increasing beta cell numbers have potential to restore blood glucose control in either type of diabetes.

To identify novel strategies for enhancing beta cell mass and function, we have sought to better understand how these processes normally occur during adaptation of beta cells to metabolic challenges. Prolonged changes in energy balance alter insulin demand and evoke coordinated adjustments to the number and function of beta cells. Thus, our studies have converged upon the roles of metabolic signaling in the adaptive processes of (1) beta cell proliferation and (2) enhancement of the insulin secretory response. Thus far, we have uncovered novel regulators of both beta cell replication as well as insulin secretion.

The Sander laboratory studies beta cell biology by employing genetic mouse models, animal physiology, genomics, and metabolomics. We have interrogated the roles of pathways of interest in beta cell adaptation to metabolic challenges using mouse models whose beta cells have been challenged through dietary, genetic, or pharmacological interventions. Future studies will assess the potential therapeutic value of modulating pathways of interest by investigating the effects in mouse models of diabetes. Furthermore, we will utilize genomic studies to determine the molecular mechanisms linking gene regulation to beta cell phenotypes (e.g. proliferation and insulin secretion). Through integration of our lab’s expertise in beta cell biology and genomics, we take a systems level approach to investigate the effect of gene perturbations on beta cell function.

Students will have the opportunity to play an important role in this exciting project. The student will work closely with scientists in the lab to generate mouse models of diabetes and monitor disease progression. Students will characterize various aspects of beta cell biology in these models, including determination of insulin secretion, monitoring beta cell proliferation, performing genomic studies, and assessing responsiveness to nutritional or signal transduction pathways. In parallel with mouse studies, culture models that mimic the diabetic environment will be utilized, enabling the application of cell culture tools such as CRISPR-Cas9 as well as validation in human beta cells. Through this experience, the student will learn techniques in animal physiology, endocrinology, molecular biology, and next generation sequencing. If interested, students will have the opportunity to interact with bioinformaticians to interrogate next generation sequencing data.

Requirements

• • Previous laboratory and rodent handling experience is highly advantageous

Contact Information

Maike Sander

Sanford Consortium for Regenerative Medicine

masander@ucsd.edu

Overview

1. Mechanisms of cortical-striatal atrophy in HD
   1. We focus on the investigation of axonal trafficking and signaling of BDNF in mouse models of Huntington's disease (HD). Our studies have demonstrated that defective axonal transport of BDNF in cortical neurons contributes significantly to striatal atrophy in HD. More importantly, we have shown that TRiC chaperonin has a protective role against axonal toxicity induced by mutant Huntingtin
2. Axonal dysfunctions in Tauopathies
   1. Tau is a microtubule associated protein (MAP). Hyper-phosphorylation or mutations in many sites on Tau are believed to contribute to its significant neurotoxicity. Using human neurons differentiated from iPS cells derived from human Tauopathy patients, we are interested in understanding: 1:  how pathogenic Tau species affects axonal transport of neurotrophic factors such as BDNF; and 2: if and how pathogenic Tau can spread via axons from neurons to neurons, or from gila to neurons, or vice versa
3. Molecular and cellular mechanisms of CMT2B peripheral sensory neuropathy
   1. Charcot-Marie-Tooth disease type 2B (CMT2B) is caused by autosomal dominant mis-sense mutations of the small GTPase Rab7 in people. We will investigate, both in vivo and in vitro, the hypothesis that CMT2B Rab7 mutation(s) causes hyper-activation of Rab7 and disrupts axonal trafficking and signaling of neurotrophic factors, leading to axonal degeneration of peripheral sensory neurons. The hypothesis is built on our in vitro studies published previously (Zhang et al., 2013, J Neurosci. 33:7451-62); and our strong preliminary in vivo results of the first ever mouse model of CMT2B, demonstrating sensory dysfunction in a knockin mouse model. In addition, we have obtained human CMT2B fibroblasts together with their control cells.  We plan to convert these cells into sensory neurons using the recently developed technologies by our collaborator Dr. K Baldwin at TSRI. By carefully examining the animal model, studying the cellular and molecular mechanisms in both animal neurons and human neurons, we will gain significant insights into the pathogenic mechanism(s) of CMT2B towards potential therapies for this debilitating disease.
4. Molecular and cellular mechanisms of HSAN V
   1. Hereditary Sensory and Autonomic Neuropathy V (HSAN V) is associated with a naturally occurred autosomal recessive mutation in NGF, discovered in a Swedish family whose patients suffer from selective loss of sensation to deep pain.  In this project, we will investigate and characterize the signaling mechanisms of this novel NGF mutant both in vitro and in vivo.  We will study how the mutation alters NGF’s ability to signal through TrkA and/or p75.  Our preliminary studies support the hypothesis that the mutant NGF retains its ability to signal through TrkA while no longer engaging the p75-mediated signaling pathways. We are actively exploring the potential use of this novel NGF mutant for treating peripheral sensory neuronal degeneration such as diabetic neuropathy, CHEMO- and HIV-induced neuropathy.

Contact Information

Chengbiao Wu

Department of Neuroscience

chw049@ucsd.edu

Overview

Human Immunology laboratory with emphasis in T cell recognition and immunotherapy design. Current focus is the role of natural regulatory T cells that recognize the heavy constant region of immunoglobulins in down-regulating inflammation.

Techniques involved: flow cytometry, culture of primary cells, ELISA.

Contact Information

Alessandra Franco

Pediatrics

alfranco@ucsd.edu

Overview

My laboratory performs research in the field of otology, specializing in the characterization, treatment and prevention of hearing loss.  This includes studies on the molecular mechanisms of damage to sensory cells and neurons in the inner ear, with the aim of identify potential therapies.  We also use screen compound libraries using cochlear tissue from transgenic mice in which the inner ear sensory cells selectively express GFP.  We are performing a human genome-wide association study to identify genes associated with tinnitus and hearing loss. In addition to our neuroscience research, we study the molecular substrates of pathogenesis and recovery in otitis media (ear infections), using gene knockout models and single-cell transcriptomics to identify inflammatory and innate immune defense genes that are active in this disorder.  Finally, we investigate novel methods for drug delivery to the middle and inner ears, including a newly discovered mechanism that actively transports particles across the intact tympanic membrane.

Contact Information

Allen F. Ryan

Departments of Surgery/Otolaryngology and Neurosciences

aryan@ucsd.edu

Overview

Our laboratory focuses on determining the genetic and molecular signals for physiological mechanism of neural plasticity and ventilatory acclimatization to chronic hypoxia. We study healthy people from sea level and adapted to high altitude in the Andes and Tibet, as well as patients with chronic lung disease and animal models, including transgenic mice. These studies are relevant to lung disease causing chronic sustained hypoxia and chronic mountain sickness, and sleep apnea that causes intermittent hypoxia. We are especially interested in mechanisms of susceptibility and tolerance to chronic hypoxia in microcircuits that control breathing in the central nervous system.

Our recent physiology experiments study:

• The effects of HIF-1α versus HIF-2α in neurons versus glia for plasticity in the CNS with chronic hypoxia.
• The role of glia and inflammatory signals in acclimatization to chronic hypoxia.

• Plasticity in the control of breathing in patients with chronic hypoxemia from lung disease.

We study the problem at multiple levels in animal models with experimental approaches including:

• measuring ventilatory responses, metabolism and respiratory muscle activity in conscious, freely moving, instrumented rats and transgenic mice,

• temporally and spatially specific conditional gene deletion using loxP-Cre strategies in transgenic mice,

• neurophysiological studies of chemoreceptor reflexes in anesthetized rats and mice

• in vivo and confocal fluorescent imaging, immunohistochemistry and molecular biological measures of signals for neural plasticity.


We also study the genetic determinants of individual variation in the hypoxic ventilatory response, including ADAPTATIONS in human populations native to high altitude in Peru and Tibet. In addition to measuring ventilatory responses, respiratory gas exchange and functional MRI in humans during acclimatization to hypoxia at high altitude, genetic studies include:

• Shared and unique genetic adaptations and physiological traits exhibited in different highland populations.
• The effects of hemoglobin concentration on oxygen transport, sleep, and gene expression at high altitude.
• The effects of sleep treatments at high altitude.
• The role of HMOX in regulating hemoglobin concentration and ventilatory control in highland populations.

For more information please see Frank Powell and Tatum Simonson’s on the  Division of Physiology website (under “People” tab) or the Center for Physiological Genomics of Low Oxygen (CPGLO) website .

Requirements

• Course in physiology preferred

Contact Information

Frank L. Powell

Division of Physiology

fpowell@ucsd.edu

Overview

The Dr. Stephen Spector laboratory has used molecular and Immunologic approaches to study host-virus interactions of human cytomegalovirus (CMV) and human immunodeficiency virus type-1 (HIV-1) with a particular emphasis developing novel approaches for the detection, treatment and eradication of persistent viruses. Current CMV related research is examining the role of CMV in endothelial cell inflammation and the development of cardiovascular diseases. The laboratory has been involved with HIV/AIDS research since the beginning of the epidemic. Current research examines HIV pathogenesis with a particular emphasis on host-virus interactions, and the associations of host genetic variants on HIV diseases progression and HIV-related diseases including CNS impairment in children and adults. The laboratory has also identified specific host genetic variants that are associated with mother-to-child transmission, HIV disease progression, and antiretroviral pharmacokinetics and adverse effects. The laboratory’s interest in the identification of host factors that affect HIV pathogenesis and neurocognitive impairment led to the novel finding that during permissive infection, HIV down-regulates autophagy to promote its own replication, and the induction of autophagy (using mTOR inhibitors as well as vitamin D3) inhibits HIV replication. Most recently, Dr. Spector’s laboratory has discovered that a Na+/K+-ATPase dependent mechanism of autophagy, termed autosis, has the potential to preferentially kill HIV persistently infected cells. This research has led to him to examine the association of host factors that control HIV replication with the goal of identifying novel strategies to eradicate HIV in order to cure persons infected with HIV.

What type of activities will you assign to your research assistant?

FMP students will work closely with a postdoctoral fellow or Research Scientist in the laboratory. Students will learn how to grow cells in culture and basic molecular biology techniques including extraction of DNA, RNA and proteins, PCR, western blots, immunostaining, etc. It is hoped that by end of the first semester students will have learned sufficient techniques to begin working on their own research project under the guidance of Dr. Spector and their direct laboratory research mentor. Many students have gone on to complete a Master’s thesis in the laboratory as part of the BS/MS program before entering medical school or pharmacy school.

Requirements

• Students must have GPA 3.5 or higher to be considered for the lab.

Contact Information

Stephen A. Spector

Division of Infectious Disease

saspector@ucsd.edu

Overview

1. Role of IFN in promoting cancer stem cells
2. Role of the cancercell in producing cytokines and initiating immune responses
3. Role of cell-cell fusion in cancer progression
4. Role of the cytokine IL-17D in antitumor and antiviral immunity

Requirements

• Need to have cell culture experience

Contact Information

Jack Bui

Medical Cancer Center

jbui@mail.ucsd.edu

Overview

Our lab uses advanced, quantitative neuroimaging and genomic data to predict response to therapy and surgical outcomes in patients with refractory epilepsy and brain tumors.  We are seeking an upper-level student with a strong background in neuro-anatomy to help with several imaging-related projects, including:

1. Radiogenomics of low-grade gliomas
2. Prediction of cognitive outcomes and white matter changes in patients with brain tumors undergoing radiotherapy 3. Using deep learning to predict true progression versus pseudo-progression in patients with malignant gliomas 4.  Multimodal imaging for the prediction of cognitive and seizure outcomes following different surgical procedures

Primary responsibilities will include managing a RedCap database of imaging and clinical information on patients with brain tumors or epilepsy, assisting with the creating of regions-of-interest on MRI scans, and for students with a programming background, working with a biomedical engineer to analyze imaging data.  Students will have exposure to a range of clinicians and researchers, including engineers, neuroradiologists, neuropsychologists, and radiation oncologists through regular lab meetings.

Requirements

• Must be able to commit to 10 hours per week, 1-2 days per week for at least 1-year
• Experience or formal coursework in neuro-anatomy, and some programming skills (Matlab, python, and R) are required
• We are particularly interested in students who have a long-term goal of conducting clinical research or aspire to develop their own project within our lab after the initial year

Contact Information

Carrie McDonald

Center for Multimodal Imaging and Genetics (CMIG)

camcdonald@ucsd.edu

Overview

Title of Project: Investigation of Cell Death Response to Cancer Drugs

Synopsis: We are interested in understanding the functions of PUMA/BBC3 (project 1) and FEN1 (project 2) in the death response of cancer cells to conventional as well as novel cancer drugs. Students will be under the direct supervision of Professor Wang to design, conduct and interpret experiments that use cell biology, molecular biology, biochemistry and genetics approaches. Specifically, students will learn basic as well as advanced techniques, including CRISPR/CAS9-mediated gene editing.

Requirements

• GPA > 3.0
• Coursework in Molecular Biology (BIMM100) and Cell Biology (BICD110) required.
• Coursework in Biochemical Techniques (BIBC103) and Recombinant DNA Techniques (BIMM101) preferred.
• Previous experiences in cell culture, western blotting and PCR preferred.

Contact Information

Jean Y. J. Wang

Department of Medicine

jywang@ucsd.edu

Overview

My lab focuses on the influence of pathogens and microbiome specifically on mast cell phenotypes with the long-term goal of demonstrating that mast cell and bacteria interactions are the keys to control skin inflammation and tolerance. The control of skin inflammation is also part of the lab interest in Rosacea. Because the control of inflammation is mediated by the mast cell release of interleukins, the lab is also studying how the TLRs – bacteria interaction can modify mast cell production of interleukins and the possible intracellular second mediators.

Some translational projects are also carried in the lab with a focus on skin diseases like Rosacea and atopic dermatitis, specifically on the role of mast cells and skin barrier have on these diseases.

Requirements

• Knowledge of basic techniques in the lab like qPCR, DNA and RNA extraction use of CRISPR/CAS, si and shRNA.
• Knowledge of the use of bioinformatics software is preferred.

Contact Information

Anna Di Nardo

Department of Dermatology

adinardo@ucsd.edu

Please copy dgarvais@ucsd.edu when contacting the Di Nardo lab.

Overview

The Hangauer lab focuses on cancer “persister” cells, a recently identified subpopulation of cancer cells found within melanoma, breast, lung, ovarian and other cancers. Persister cells reversibly enter a quiescent, pro-survival cell state and avoid drug-induced cell death through poorly understood mechanisms. The distinguishing feature of persister cell biology is the persister cells’ reversible drug resistance which indicates that these cells initially utilize non-genetic/non-mutational mechanisms to survive. Importantly, these cells can form a long term surviving cancer cell reservoir from which drug-resistant tumors may ultimately emerge.

Project 1: Exploration of whether cancer “persister” cells acquire drug resistance-conferring genetic mutations that allow resistant tumors to emerge. This project consists of utilizing cell culture and molecular biology techniques including CRISPR, RNAi, western blotting, qPCR, deep sequencing, fluorescence microscopy and cell viability assays to explore this question.

Project 2: Identification of novel therapeutic target genes within cancer persister cells. This project consists of performing high throughput CRISPR and/or small molecule chemical screens in cultured cancer “persister” cells to identify novel gene therapeutic targets and/or drug leads.

Requirements

• Prior experience with mammalian cell culture preferred.

Contact Information

Matthew Hangauer

Department of Dermatology

mhangauer@ucsd.edu

Overview

The Lab of Prof. Gerry R. Boss from the School of Medicine is seeking one student interested in performing their BS/MS studies in pharmaceutical sciences and drug discovery. In particular, the BS/MS candidate will work with a postdoctoral fellow, Dr. John Tat. Together, this mentor-mentee team will utilize biochemical, cellular, and physiological techniques to delineate the mechanism of toxicity for azide, a toxic chemical that has been listed as a potential weapon of mass destruction. The team will also test whether drugs developed by Prof. Boss’ group could be used as antidotes for treating acute azide poisoning. This study is translational in nature and has both clinical and public health values.

Requirements

• Upper-division major GPA 3.3+
• Must be able to commit 10-12 hrs a week during BS portion
• Must be willing to work with mammalian cells, D. melanogaster, and mice
• Coursework
  • BIBC 102 – Metabolic Biochemistry
  • BIBC 103 – Biochemical Techniques
  • BICD 110 – Cell Biology
  • BIPN 100 – Human Physiology I
• Required techniques
  • Experience with mammalian tissue culture
  • Experience with SDS-PAGE and western blotting

Contact Information

To apply: Interested candidates please contact Dr. John Tat at johntat@ucsd.edu and submit a CV, an unofficial transcript, and the names of two to three professional references.

Research in the Hook Lab

Research in the Hook laboratory investigates molecular mechanisms of neurological diseases for elucidation of drug targets for therapeutics discovery. The hypothesis being studied is that dysfunction in synaptic neurotransmission occur in brain disorders, involving proteases in cell-cell communication and cell death. Advances technologies in molecular to neurochemical, proteomics, cellular and tissue pathology in disease models and clinical human tissues are utilized.

Current Projects Open for BS/MS Students

1. Novel therapeutics for treatment of chronic pain without addiction, by targeting reduction in expression of the dynorphin neurotransmitter. Antisense agents to reduce dynorphin gene expression in cultured cells and rodent models are being development for treatment of chronic pain.
2. Huntington's Disease (HD) gene variants lead to alterations in proteomics of human brain systems. Human HD brain tissues are being investigated for analyses of proteomics changes in molecular pathways resulting from genetic mutation variants of the HTT gene in HD.

Requirements

• Committment and motivation to advance progress in the research project.
• Course background in molecular and cell biology, biochemistry, and cell biology are desired.

Contact

Vivian Hook

Skaggs School of Pharmacy and Pharmaceutical Sciences

vhook@ucsd.edu

Overview

We are both a wet lab and systems/computational biology lab interested in a variety of biomedical problems. A number of BS-MS students have trained here. One major focus is on the systems biology of drug and endogenous metabolite transport. We are particularly interested in the role of drug transporters in inter-organ and inter-organismal (eg. microbiome-host) communication via metabolites and signaling molecules. We also study organ development and tissue engineering, particularly relating to the kidney.

Current Projects

• Creating a Transporter Based Metabolic Network
  • This project focuses on discovering the role of transporter membrane proteins in normal metabolic and signaling pathways. Some of these proteins have been identified by the FDA because of their importance in the excretion of drugs, but recently, they have been hypothesized to play a role in much broader role in metabolism. By studying the known shared substrates between these proteins, we are developing a network that elucidates how these proteins work together to maintain homeostasis in health and disease states.
• Evolutionary Analysis and Functional Elucidation of “Drug Transporters”
  • Many small molecule transporters are known only for their role in pharmacological settings. This project traces these transporters back to model organisms in hopes of establishing a classification of endogenous function that could be utilized in maintaining homeostasis and in turn, improve and expand upon the current ideology surrounding the pharmaceutical implications of these transporters. This project utilizes bioinformatics techniques as well as wet-lab assays.
• Making Transporter-Mediated Drug-Metabolite Interaction Predictions
  • Research focused on the involvement of SLC transporters in physiological metabolism and pharmacology by comparing the relationship between drug space and metabolite space of OAT1 and OAT3. These analyses help to further understand the multispecific features of the “drug” transporters and how drug-induced metabolic syndrome arises during chronic treatment. This project utilizes computational biology and cheminformatics techniques as well as wet-lab assays.
• Organ development and Tissue Engineering
  • We work on many aspects of prenatal and postnatal kidney development using in vitro and in vivo models. We are particularly interested in developmental approaches to organ engineering.

Lab Environment

The Nigam Lab is located on the first floor of the Leichtag Family Foundation Biomedical Research Building at UCSD Medical School. We are currently educating 1 PhD student and 2 Masters students.

Requirements

• GPA requirement is that of the BS/MS program
• Biology/Biochemistry/Bioengineering majors or minors
• Must be able to commit ~15 hours/week as an undergraduate
• Some wet lab experience in molecular biology, cell biology, or physiology in cells or model organisms (this includes coursework such as BIMM101, BIPN105, or BIBC103)
• Must be independently motivated, and interested in health sciences, pharma or biotechnology

Contact

Sanjay Nigam, MD

Pediatrics and Medicine

snigam@ucsd.edu