Photo of Fred L. Robinson, Ph.D.

Fred L. Robinson Ph.D.

  • (503) 494-8783
    • Assistant Professor of Neurology School of Medicine
    • Joint Appointment Vollum Institute
    • Jungers Center for Neurosciences Research
    • Biochemistry and Molecular Biology Graduate Program School of Medicine
    • Neuroscience Graduate Program School of Medicine
    • Program in Molecular and Cellular Biosciences School of Medicine

Fred Robinson, Ph.D., joined the Jungers Center as an assistant scientist and assistant professor of Neurology in August 2009. Dr. Robinson received an undergraduate degree at Oregon State University in biology and genetics, and a master’s degree in biological sciences from the University of Nebraska-Lincoln. After graduate training in Biochemistry at UT Southwestern with Melanie Cobb, he joined the laboratory of Jack Dixon at the University of California, San Diego in 2002. Dr. Robinson is a recipient of a prestigious NIH Pathway to Independence Award, which will facilitate the development of his laboratory in the Jungers Center. He holds a joint appointment in the Vollum Institute.

Areas of interest

  • Glial cell biology
  • Myelination
  • Phosphoinositide signaling
  • Membrane trafficking and dynamics
  • Axonal degeneration
  • Charcot-Marie-Tooth disease
  • Peripheral neuropathy

Education

  • Ph.D., University of Texas Southwestern 2002
  • Fellowship:

    • Postdoctoral Fellow, University of California at San Diego, 2002-2009

Publications

  • "Schwann cell-specific deletion of the endosomal PI 3-kinase Vps34 leads to delayed radial sorting of axons, arrested myelination, and abnormal ErbB2-ErbB3 tyrosine kinase signaling." GLIA In: , 2017.
  • "The CMT4B disease-causing phosphatases Mtmr2 and Mtmr13 localize to the Schwann cell cytoplasm and endomembrane compartments, where they depend upon each other to achieve wild-type levels of protein expression." Human Molecular Genetics In: , Vol. 22, No. 8, 04.2013, p. 1493-1506.
  • "Sbf/MTMR13 coordinates PI(3)P and Rab21 regulation in endocytic control of cellular remodeling." Molecular Biology of the Cell  In: , Vol. 23, No. 14, 15.07.2012, p. 2723-2740.
  • "Loss of the inactive myotubularin-related phosphatase Mtmr13 leads to a Charcot-Marie-Tooth 4B2-like peripheral neuropathy in mice." Proceedings of the National Academy of Sciences of the United States of America In: , Vol. 105, No. 12, 25.03.2008, p. 4916-4921.
  • "Myotubularin phosphatases : policing 3-phosphoinositides." Trends in Cell Biology In: , Vol. 16, No. 8, 08.2006, p. 403-412.
  • "The phosphoinositide-3-phosphatase MTMR2 associates with MTMR13, a membrane-associated pseudophosphatase also mutated in type 4B Charcot-Marie-Tooth disease." Journal of Biological Chemistry In: , Vol. 280, No. 36, 09.09.2005, p. 31699-31707.
  • "The Death Effector Domain Protein PEA-15 Prevents Nuclear Entry of ERK2 by Inhibiting Required Interactions." Journal of Biological Chemistry In: , Vol. 279, No. 13, 26.03.2004, p. 12840-12847.
  • "Identification of novel point mutations in ERK2 that selectively disrupt binding to MEK1." Journal of Biological Chemistry In: , Vol. 277, No. 17, 26.04.2002, p. 14844-14852.
  • "MAP kinases." Chemical Reviews In: , Vol. 101, No. 8, 08.2001, p. 2449-2476.
  • "Hydrophobic as well as Charged Residues in both MEK1 and ERK2 are Important for their Proper Docking." Journal of Biological Chemistry In: , Vol. 276, No. 28, 13.07.2001, p. 26509-26515.
  • "Mitogen-activated protein (MAP) kinase pathways : Regulation and physiological functions." Endocrine Reviews In: , Vol. 22, No. 2, 2001, p. 153-183.

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