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  • Xuebiao Yao, Ph.D.

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  • Xuebiao Yao, Ph.D.
      Professor, Department of Physiology


    Contact Information
    Phone: (404)752-1894
    Fax: (404) 752-1045
    Email: xyao@msm.edu
    Education B.S., Jiangxi College of Medicine, China (Medicine/Pharmacology)
    Ph.D., University of California-Berkeley (Molecular Cell Biology)
    Postdoc, University of California-San Diego (Cancer Cell Biology)

    Research Interests
    Cellular polarity in health and diseases: Rho-family GTPases, including Cdc42, Rac1 and RhoA, regulate actin cytoskeleton and cell adhesion and are implicated in cell polarisation in several cell types, including T cells, fibroblasts, macrophages, astrocytes, epithelial cells and neuronal cells. Our research objectives are directed to understand cellular mechanisms involved in establishment and maintenance of cell polarity using gastric epithelial cells as a model system.

    Many protein complexes required to establish and maintain epithelial function and structural integrity are polarized epithelial cells. Recent studies in gastric cell culture and in animal demonstrate the functional importance of ezrin in establishment and maintenance of gastric parietal cell polarity. One avenue of our current efforts is directed to evaluate the organization, assembly and function of the ezrin protein complex in epithelial cell plasticity.

    Helicobacter pylori persistently colonize the human stomach and have been linked to atrophic gastritis and gastric carcinoma. Although it is well known that H. pylori infection can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood. We have recently demonstrated that VacA permeabilizes the apical membrane of gastric parietal cells and induces hypochlorhydria. Currently, we are examining how Helicobacter pylori cytotoxins such as VacA perturb genomic stability of gastric parietal cells using a novel 3D culture system.

    Mitotic chromosome segregation and genomic stability: During cell division, each daughter cell inherits one copy of every chromosome. Accurate transmission of genetic materials (chromosomes) requires that the sister chromatids are disentangled and then segregated toward opposite poles of the cell before division.  Defects in chromosome segregation produce cells that are aneuploid (containing an abnormal number of chromosomes).  Aneuploidy is a leading cause of spontaneous miscarriages in humans and is also a hallmark of many human cancer cells.

    Kinetochore, a multi-protein super-structure, mediates attachment of chromosomes to the mitotic spindle and governs complex chromosome movements during cell division.  In addition to mediating the mechanical process of chromosome segregation, kinetochores integrate the interaction of the mitotic spindle with chromosome in cell cycle progression.  Kinetochore serves as surveillance machinery for a 'checkpoint' in this process, termed spindle assembly checkpoint, a signaling pathway that ensures the fidelity of chromosome segregation.  Currently, we are delineating how protein-protein interactions at the kinetochore is orchestrated during cell division and what happens when specific protein-protein interaction is perturbed in real-time live cells using optical reporters.

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