School of Medicine


Showing 21-40 of 42 Results

  • 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.

Footer Links:

Stanford Medicine Resources: