School of Medicine


Showing 1-39 of 39 Results

  • Andrew Nager

    Andrew Nager

    Postdoctoral Research Fellow, Molecular and Cellular Physiology

    Current Research and Scholarly Interests A decade ago, a collection of multi-organ pediatric disorders was attributed to dysfunctional cilia; cell-surface organelles that mediate cell-to-cell communication. These disorders (termed ciliopathies) predispose patients to respiratory inflammation, diabetes, and cancer, and the elucidation of cilia functions inform these prevalent health problems. Reflecting the diverse symptoms of cilia diseases, cilia function throughout the body, and surprisingly, almost every cell type presents at least one cilium. Cilia house receptors and receive signals, but it is not known how signaling is regulated or transduced into the cell. Receptor trafficking provides a molecular entry point to this problem as the receptor mistrafficking is characteristic of ciliopathies. The goal of my research is to determine how receptor trafficking regulates cilia signaling, and to uncover novel roles of cilia in cell-to-cell communication.

    1. Receptor Trafficking and Bardet-Biedl Syndrome
    The ciliary membrane contains numerous G-protein coupled receptors (GPCRs) that, upon activation, are removed from the cilium. By live-cell imaging of ciliated epithelial cells, I found that two competing pathways remove activated GPCRs from cilia: retrieval back into the cell or secretion into extracellular vesicles. Importantly, in the ciliopathy Bardet-Biedl Syndrome (BBS), both pathways are misregulated. One branch of my research focuses on how BBS-associated proteins regulate receptor trafficking, and how receptor trafficking regulates signaling.

    2. Biogenesis of Extracellular Vesicles
    A second thrust of my research is to understand how extracellular vesicles are formed. Extracellular vesicles are widely observed in biology, and function both to dispose unwanted molecules and transfer messages to other cells. Mammals release extracellular vesicles by several distinct pathways, yet our molecular understanding is limited to highly-conserved components identified by yeast genetics. Although yeast genetics discovered the important ESCRT cascade, mammals have elaborated and, in some contexts deviated from, this mechanism. For instance, mammalian cells have evolved to use actin for releasing vesicles from cilia, microvilli, and the plasma membrane. Leveraging biochemical tools for studying cilia, I identified a network of actin motors (Myosin 6) and crosslinkers (Drebrin, alpha-Actinin-4) that sever extracellular vesicles from cilia. This research informs how mammals produce extracellular vesicles, and provides molecular tools to determine the physiologic functions of extracellular vesicles.

  • Yusuke Nakauchi M.D., Ph.D.

    Yusuke Nakauchi M.D., Ph.D.

    Postdoctoral Research Fellow, Stanford Cancer Center

    Current Research and Scholarly Interests From 2005 to 2010, my work as a clinical hematology fellow allowed me to experience first-hand how scientific advances that started in a laboratory can transform the lives of patients. While many of my patients were cured of their disease with allogeneic hematopoietic stem cell transplantation, underscoring the importance of anti-tumor immunotherapy in eradicating leukemia, I witnessed face-to-face their suffering from the long-term consequence of graft-versus-host disease (GVHD). This experience was ultimately what drove me to engage in research to discover novel therapies. For this reason, I embarked on a PhD program in 2010 to design antibody therapy to (i) target GVHD and (ii) target hematological malignancies. Under the mentorship of Professor Hiromitsu Nakauchi at the University of Tokyo, an international leader in hematopoiesis, I developed allele-specific anti-human leukocyte antigen (HLA) monoclonal antibodies for severe GVHD caused by HLA-mismatched hematopoietic stem cell transplantation (Nakauchi et al., Exp Hematol, 2015). This study was the first to find that anti-HLA antibodies can be used therapeutically against GVHD. That success gave me the motivation and confidence to further my research beyond targeting GVHD, to targeting leukemic stem cells through my current postdoctoral fellowship in the laboratory of Professor Ravindra Majeti, Department of Hematology at Stanford University.

    Many people suffer from leukemia each year, but we still don?t know how to completely cure it. Recent advances in sequencing technologies have tremendously improved our understanding of the underlying mutations that drive hematologic malignancies, although, the reality is that the majority of the mutations are not easily ?druggable? and the discovery of these mutations has not yet made a significant impact in patient outcomes. I view this perhaps the most crucial challenges facing a translational cancer researcher like myself. My current research is a major step toward my long term goal to make personalized medicine a reality for patients with acute myeloid leukemia (AML) and other hematologic malignancies. Although my research is focused on targeting Ten-Eleven Translocation methylcytosine dioxygenase-2 (TET2) mutations, I anticipate it will lead to a better understanding of the cell context requirement for TET2 mutations in AML and help identify the critical cells to target to both prevent the development of de novo leukemia and halt relapse. It may also prove of value to understanding of the biology of a range of other cancers.

  • Vivek Nanda

    Vivek Nanda

    Postdoctoral Research Fellow, Vascular Surgery

    Bio I am interesting in identifying the heritable component of a wide range of cardiovascular diseases which include coronary artery disease and peripheral artery disease. To this end, I am involved in utilizing genome-wide genetic and bioinformatics approaches to identify loci responsible for disease, and thereafter validating these findings by implementing a variety of molecular genetics, molecular biology and transgenic mouse models to explain the vascular biology of the identified gene or pathway.

  • Valerio Napolioni, PhD

    Valerio Napolioni, PhD

    Postdoctoral Research Fellow, Neurology and Neurological Sciences

    Current Research and Scholarly Interests My research is focused on the genetic underpinnings of common complex neuropsychiatric disorders with an emphasis on evolutionary/adaptive effects of gene variants. Given the incredible complexity underlying human neurobehavioral traits, I strongly believe in the necessity of applying a multidisciplinary approach that may involve genetics, neuropsychiatry, ecology, immunology and sociology. Currently I?m working on X-chromosome wide association studies, aiming to get a better understanding of sex-specific differences in the susceptibility to neuropsychiatric conditions.

  • Gernot Neumayer

    Gernot Neumayer

    Postdoctoral Research Fellow, Stem Cell Biology and Regenerative Medicine

    Current Research and Scholarly Interests My MSc project, carried out at the University of Salzburg in cooperation with the biotechnology company ProComCure, investigated the molecular interface between human cells and the bacterium Staphylococcus aureus. S. aureus exhibits a dramatic increase in resistance to antibiotics, thereby causing enormous challenges for health care. Using proteomics platforms, I identified numerous novel host-pathogen interactions. These findings are being developed further by ProComCure in order to design innovative therapies for S. aureus infections.

    My dissertation project, carried out at the University of Calgary, defined the functions of the human protein TPX2. TPX2 has been discovered over 17 years ago for its unique property to mediate cell division. However, when not involved in cell division TPX2 resides in the cell nucleus where its role had remained unknown. Building on my background in proteomics, I discovered a novel TPX2-containing protein complex that resides in the nucleus. Analysis of this complex unraveled a completely unexpected role for TPX2 in cellular reactions triggered by insults to DNA. To avoid cancers, cells respond to damaged DNA by either attempting its repair or, if this is not possible, by committing 'suicide'. My findings established that TPX2 impacts the molecular mechanisms that underlie these responses to DNA damage. More specifically, I found that TPX2 accumulates at DNA lesions and that the cellular levels of TPX2 negatively correlate with the ?strength? of the DNA damage response. Thus, TPX2 affects cellular proliferation, DNA repair, and survival upon genomic insult. This was the first function discovered for TPX2 in the cell nucleus. Since abnormally high levels of TPX2 are often found in human cancers, my discovery sheds light on the mechanistic implication of this protein in carcinogenesis. Furthermore, TPX2 is also a promising therapeutic target and my findings may advance novel cancer therapies. We propose that future treatments may attempt to reduce TPX2 levels in order to increase the strength of the DNA damage response. Subsequently, chemo- and radiotherapy doses may be lowered but still stay effective.

    In 2014, I joined the Wernig laboratory at Stanford University. Here, I capitalize on my expertise in mechanisms of DNA damage response to develop a pioneering technique capable of repairing pathogenic mutations in the genetic material of patients suffering from Epidermolysis Bullosa (a devastating and often lethal disease that causes chronic erosion of the skin). This novel technique, called CRISPR, introduces experimentally controlled and transient damage to the mutated DNA of patient cells and exploits naturally occurring DNA repair mechanisms to transform the disease-causing mutation to a normal state. I will combine development of CRISPR with Dr. Wernig?s expertise in regenerative medicine to generate patient derived stem cells with repaired (i.e. normal) genes. Subsequently, these stem cells will be employed to regenerate the skin of Epidermolysis Bullosa patients.

  • Khoa D Nguyen

    Khoa D Nguyen

    Postdoctoral Research Fellow, Pathology

    Current Research and Scholarly Interests Neuroscience
    Immunology
    Innate Immunity
    Metabolism

  • Toshinobu Nishimura

    Toshinobu Nishimura

    Postdoctoral Research Fellow, Stem Cell Biology and Regenerative Medicine

    Current Research and Scholarly Interests In my undergraduate and graduate school, my research interests are in the development of bloods cells especially immune cells from hematopoietic stem cells (HSCs). As an undergraduate, I conducted research with Dr. Hitoshi Sakano on elucidating the mechanism of the diversification of the immune receptors in jaw-less animals (more primitive species than fish) such as sea lamprey and hagfish. Sea lamprey and hagfish has different type of immune receptor gene from T-cell receptor (TCR) or Immunoglobulin (Ig), and gene assembly other than V(D)J recombination occurs on the gene for diversifying it. By using immunogenetics, molecular biology, and computational method I uncovered the way for diversifying the immune receptor gene in these species.

    I switched my research field to rodents in my former half of Ph.D. course. With Dr. Hiromitsu Nakauchi I focused on generating transplantable HSC from mouse embryonic stem cells (ESCs). I could purify and phenotyped the population which have the capacity for engrafting and repopulating in mouse bone marrow after transplantation. In latter half of Ph.D. course, I combined my knowledge about immunology with HSC induction technique for generating immune cells from human induced pluripotent stem cells (iPSCs). I succeeded to obtain abundant and highly functional antigen-specific T cells from human iPSCs, along with rejuvenating the exhausted state by passing through iPSC-reprogramming and redifferentiation.

    For research in postdoctoral fellow, I choose to generate 3D organs from human iPSCs. It is very challenging theme but I?m thinking my experiences, knowledge, and techniques in pluripotent stem cells should bear fruit. I continue the T-cell generation research and I?m planning to translate the T-cell products to clinic.

  • Jonathan Nizar

    Jonathan Nizar

    Clinical Instructor, Medicine - Nephrology

    Current Research and Scholarly Interests Diabetes and hypertension are among the most common diseases treated in the US. The combination of these disease greatly increased the risk of heart attack, stroke, and early death. While over 90% of patients with diabetes have high blood pressure, its cause is unknown. Working in the laboratory of Vivek Bhalla, I am interested in understanding the mechanisms that diabetes contributes to high blood pressure. We current are focused on the regulatory role of insulin on sodium reabsorption in the kidney, which is a master regulator of blood pressure. Using a mouse model of diabetes and transgenic technologies, we utliize classical metabolic experiments, expression, electrophysiological, and primary cell culture techniques to understand the role of insulin in regulating sodium transport in the kidney, blood volume in the body, and increased blood pressure in diabetes.

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