Philip F. Copenhaver, Ph.D.

  • Professor of Cell, Developmental and Cancer Biology, School of Medicine
  • Director, Cell and Developmental Biology Graduate Program, School of Medicine
  • Cell and Developmental Biology Graduate Program, School of Medicine
  • Neuroscience Graduate Program, School of Medicine
  • Program in Molecular and Cellular Biosciences, School of Medicine
  • Cancer Biology Graduate Program, School of Medicine


Professional Experience:

After undergraduate studies at Stanford University, Philip Copenhaver attended graduate school in the Department of Zoology at the University of Washington in Seattle, where he received his Ph.D. with Dr. James Truman in 1985. He spent three years as a post-doctoral fellow with Dr. Paul Taghert in the Department of Anatomy and Neurobiology at Washington University Medical School in St. Louis, and an additional year with Dr. William Moody at the University of Washington. He joined the Department of Cell and Developmental Biology at Oregon Health & Science University in 1990 as an Assistant Professor; was promoted to Associate Professor in 1996, and to Professor in 2011. Dr. Copenhaver currently serves as the director for the Graduate Program in Cell and Developmental Biology (CDB) and director for the Development, Differentiation, and Disease (D3) in the Program in Biomedical Sciences (PBMS). He is also a member and course director in the Neuroscience Graduate Program (NGP), and is a primary instructor for human embryology in the medical school.


Current research interests:

My research is focused on the cellular and molecular mechanisms that regulate neuronal migration during embryogenesis. For much of my work, I have used the enteric nervous system of the moth (Manduca sexta) as a simple model system for neuronal migration, which allows acute manipulations of the cellular and molecular components regulating the migratory process to be performed within the developing embryo. This preparation has proven effective in identifying evolutionarily conserved signaling pathways involved in neuronal guidance that we then test in a variety of complementary systems, including genetic manipulations in Drosophila and acute manipulations of cultured hippocampal neurons. Current projects include an analysis of the normal role of the Amyloid Precursor Protein (APP) in the brain.  APP is best known as the source of b-amyloid (Ab) peptides that have been postulated to cause Alzheimer’s disease (AD). However, therapeutic strategies targeting Ab have been unsuccessful, suggesting that other APP-related activities may contribute to the disease. To address this issue, we have adapted a combination of insect model systems (Drosophila and Manduca) that permit direct manipulations of motile neurons in vivo and in vitro.  Using a combination of biochemical, pharmacological, and genetic strategies, we have found that APP family proteins can function as unconventional G protein-coupled receptors that regulate neuronal motility via the heterotrimeric G protein Goa. Our recent studies using mammalian neurons and human brain samples from the Oregon Brain Bank have indicated that this signaling pathway is evolutionarily conserved and may be perturbed in the aging a diseased brain. In collaboration with other faculty at OHSU, we have also incorporated our model systems into integrated suite of bioassays to test compounds that may ameliorate amyloid toxicity, including clinically approved ion channel blockers and novel compounds targeting membrane estrogen receptors.  We also recently found that insect macrophages play a neuroprotective role by scavenging the shed fragments of APP-related proteins, providing a novel assay for evolutionarily conserved components of the innate immune response. Our goal is to exploit this model systems approach to define the normal regulation of APP and its signaling partners, which in turn may provide a new perspective on how these pathways are disrupted in AD. A second project addresses novel signaling mechanisms of GPI-linked Ephrins in response to Eph receptors (originally identified as oncogenes), and their modulation of Src family kinases during development and tumor invasiveness. In particular, we have recently identified a novel mechanism of ‘reverse’ signaling by GPI-linked (type-A) Ephrins; and defining the role of isoform switching in the regulation of neuronal motility by Ig-CAM receptors that requires the recruitment of the oncogenic tyrosine kinase Src. We are currently testing whether this novel signaling pathway is also required for Ephrin-dependent control of insulin secretion in mouse pancreatic islets.   A third project is focused on the role that distinct isoforms of the same neuronal guidance receptor (Fasciclin II; insect NCAM) plays in regulating different aspects of neuronal migration and axon growth within the developing nervous system.  We are also testing the role of a novel “G3BP” protein (Rasputin) in coordinating mRNA transport, expression, and Rho-GAP activity required for Fasciclin II to function correctly. Besides identifying novel components of these transduction pathways, our goal is establish a framework for testing how similar signaling mechanisms may be disrupted in developmental disorders that affect the mammalian nervous system.

Education and training

    • B.S., 1979, Stanford University
    • M.S., 1979, Stanford University
    • Ph.D., 1985, University of Washington
  • Fellowship

    • Post-doctoral fellowship, Washington University School of Medicine, St. Louis MO; 1986-1989 (Mentor: Paul Taghert, PhD)
    • Post-doctoral fellowship, University of Washington, Seattle, WA: 1989-1990 (Mentor: William Moody, PhD)

Areas of interest

  • Developmental Neuroscience
  • Mechanisms of neuronal migration
  • Neurobiology of disease
  • Simpler model systems
  • Biology of Amyloid Precursor Protein (APP)
  • Alzheimer's Disease



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