Chair:
Dale R. Abrahamson, PhD
Graduate Studies Director:
Douglas E. Wright, PhD
Director of
Medical Education:
George C. Enders, PhD
Email inquiries:
hallensw@kumc.edu
The Department of Anatomy and Cell Biology has a strong history of providing outstanding training environments for graduate students and postdoctoral scientists. Many of our trainees have gone on to positions at prestigious educational or commercial institutions. The following list provides information about alumni who have trained in the Department of Anatomy and Cell Biology.
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Anastasiia Aleksandrova Mentor: Brenda Rongish, Ph.D. aaleksandrova@kumc.edu My research project is concerned with the early stages of heart development in avian embryos. A comprehension of the processes that occur during heart formation is necessary for understanding the basis of various forms of congenital heart disease. I am interested in the forces that drive the formation of the endocardial (inner) layer of the forming heart. We are trying to understand and compare the roles of active cell migration and global tissue displacements in this process. Also, I am working on preparing the position-fate maps of endocardial cells along with several extracellular matrix molecules that play important roles in cardiac development. |
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Shachi Bhatt Mentor: Paul Trainor sbhatt@kumc.edu Research Project : Neural Crest in Mammalian Development. My research project focuses on induction of Neural Crest Cells and the role of an orphan nuclear receptor GCNF in the process. Neural Crest Cells are a transient population of multipotent and migratory cells that give rise to numerous derivatives in the vertebrate body. These cells provide an excellent model to study cell induction, migration and differentiation in the developing embryo. Neural Crest abnormalities in any of these events lead to various congenital abnormalities. Understanding the role of neural crest cells is inevitable to understand the cause and nature of these congenital defects. I would also be working on the role of a mediator subunit during embryonic development. |
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Sara Billings Mentor: Hiroshi Nishimuni, Ph.D. sbillings@kumc.edu Research interest: I am studying how cell-adhesion molecules contribute to synapse formation and organization of the active zone at the synaptic terminal. Some synaptic adhesion molecules, like neuroligin, LRRC4C and Syncam proteins, are able to induce differentiation of presynaptic terminals in cultured neurons. My primary interest is to understand how contact between these extracellular molecules and receptors on the presynaptic membrane translates into intracellular effects that lead to presynaptic differentiation. |
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Raul Diaz Mentor: Paul Trainor, Ph.D. rdiaz@kumc.edu I am interested in the evolution and development of the vertebrate skeleton. In Paul Trainor’s lab we are looking at the role of miRNA/Dicer’s role in fine tuning the development of craniofacial structures in mice (and other vertebrates) and the effect this has on neural crest cells and their derivatives. |
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Megan Dunn Mentor: Doug Wright, Ph.D. mdunn@kumc.edu Research Project: Diabetic neuropathy (DN) is a common complication of diabetes affecting over half of all diabetic patients. Patients with DN develop painful or insensate neuropathy to mechanical and thermal stimuli due primarily to small diameter sensory nerve fiber loss. However, the underlying pathophysiological mechanisms leading to the development of either positive or negative symptoms are not well understood. My current project is to characterize the expression of glyoxalase I (GloI) in mouse models of painful and insensate DN. We hypothesize differential GloI expression levels in the peripheral nervous system may lead to differences in AGE formation and modulate the development of painful versus insensate neuropathy. |
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Ashleigh Fritz Mentor: Matt Gibson, Ph.D. afritz@kumc.edu |
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Brianne Guillford Mentor: Douglas Wright, Ph.D bguilford@kumc.edu Research Project Diabetic neuropathy is one of the principle chronic complications of both type 1 and type 2 diabetes mellitus and currently affects more than half of diabetic patients. Sensory loss, including both chronic numbness and sensitivity to pain or touch, develops in the majority of affected patients. The mechanisms that lead to painful or insensate symptoms in diabetic neuropathy are poorly understood. Oxidative stress is one of many variables that have been implicated as a critical feature in diabetic neuropathy. The goal of my current project is to characterize oxidative stress in painful and insensate neuropathy and determine if antioxidants have differential effects in mouse models that vary in their oxidative stress levels. |
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Anna Groover Mentor: Douglas Wright, Ph.D. agroover@kumc.edu Research: Fibromyalgia is a complex chronic pain disorder affecting approximately 10 million people in the United States, primarily women. It is characterized by widespread pain, sleep disturbances, fatigue, abnormal tenderness and even psychological distress. While a lot is known about the symptoms of Fibromyalgia, not a lot is known about the causes or mechanisms of the disorder. The goal of my research is to look at causative factors, such as sleep deprivation, diet, aging and stress/anxiety, to determine how they affect the development and modulation of pain associated with the syndrome. I also want to look at molecular modulators, like stress kinases, which increase the pain behavior associated with Fibromyalgia. |
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Caleb Grote Mentor: Douglas Wright, Ph.D. cgrote@kumc.edu |
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Binu Paul Mentor: Greg Vanden Heuval, Ph.D bpaul@kumc.edu Research Project: My primary research goal is to explore and understand the molecular mechanisms involved in one of the life-threatening genetic diseases, polycystic kidney disease. Research in this field can lead to better treatment regimens. There is increased ectopic expression of Cux-1, a homeobox gene in both human as well as mouse models of polycystic kidney disease. Regulated expression of Cux-1 is very important during development. In one sentence, my aim is to further elucidate the role of Cux-1 in polycystic kidney disease and development. |
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Autumn Ruiz Mentor: Ed Stephens, PhD aruiz@kumc.edu Similar to other viruses human immunodeficiency virus type 1 (HIV-1) encodes several genes designed to promote replication, evade the host immune system and inhibit the functions of cellular restriction factors. One of these genes is the Viral protein U (Vpu) protein that functions to enhance virion release and down-regulate CD4 molecules from the surface of infected cells to prevent superinfection and promote virion assembly. One of the main objectives of our laboratory is to characterize the molecular mechanisms by which the HIV-1 Vpu protein contributes to viral pathogenesis using a chimeric simian-human immunodeficiency virus (SHIV) macaque model of disease. We hypothesize that different HIV-1 subtypes encode proteins with distinct biological properties that contribute to the ability of these viruses to spread within the human population. My research project focuses on the characterization of distinct biological properties and cellular protein interactions of subtype B and subtype C Vpu proteins and their effects on viral pathogenesis. |
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Kimberly Schmitt The human immunodeficiency virus type 1 (HIV-1) must overcome intracellular host defense mechanisms in order to establish infection. Both HIV-1 and other lentiviruses encode for a Vif (virion infectivity factor) protein, which is required for production of infectious virions by counteracting the innate antiviral activities of the APOBEC3 family of cytidine deaminases. Vif promotes the ubiquitination and subsequent proteasomal degradation of APOBEC3 proteins. The focus of our laboratory is to characterize molecular mechanisms utilized by the Vif protein using the simian-human immunodeficiency virus (SHIV)/macaque model of infection. My research focuses on characterizing specific domains in Vif required for both the interaction and degradation of APOBEC3G and APOBEC3F, which are known to be important in viral restriction. |
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Christopher Tanzie Mentor: Ting Xie ctanzie@kumc.edu Research Project: Notch is an evolutionarily conserved pathway essential to numerous developmental contexts. Mutations in Notch related proteins have also been shown to be the cause of various hereditary diseases and some leukemic cancers. My current project focuses on the Notch2 receptor, defects in which can result in Alagille Syndrome. One aspect of Alagille Syndrome is anterior eye defects. Using mouse as a model, we are studying the Notch2 receptor and its regulation of ciliary body proliferation and morphogenesis in the anterior eye. By incorporating standard developmental techniques with newer technologies such as Cre-loxP, bioinformatics, and cell sorting, we are discovering how Notch2 regulates ciliary body development through its interaction with other signaling pathways. |
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Le Zhan Mentor: Ron Yu lzhan@kumc.edu Research Interests: Cell and development biology & Neuroscience, especially human brain research. |
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