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Bryce  M.  Paschal
Degree(s): Ph.D.
Graduate School: University of Massachusetts
Primary Appointment: Associate Professor of Biochemistry and Molecular Genetics
Research Interests:
Nuclear Transport, Signaling, and Cancer

Email Address: bmp2h@virginia.edu


Biomedical Sciences Graduate Program(s)
  • Biochemistry, Molecular Biology and Genetics
  • Molecular Cell and Developmental Biology
  • Microbiology, Immunology and Infectious Diseases

  • Research Description

    My laboratory studies how nuclear transport and signal transduction control the compartmentalization and activity of transcription factors, particularly in the context of prostate cancer. A major focus of these studies is the androgen receptor (AR), a steroid hormone receptor that is critical for prostate cell growth. Translocation of AR through the nuclear pore complex (NPC) relies on features common to most nuclear transport pathways: (i) the use of nuclear import or export signals; (ii) the recognition of these signals by receptors that mediate translocation through the NPC; and (iii) RanGTPase-dependent assembly and disassembly of transport complexes. The signals that specify nuclear import and export of AR, the receptors that mediate AR translocation, and the role of the RanGTPase in AR transport are all under investigation in my laboratory. Nuclear export would be expected to provide an effective mechanism for terminating the transcriptional response to androgen, however, we have recently found that AR translocation to the cytoplasm is important for its activity in the nucleus. This apparent paradox may reflect an undefined step in AR maturation, or crosstalk between AR and signal transduction pathways in the cytoplasm.

    AR is the target of multiple kinases, and we have generated phosphosite antibodies to study the pathways and functions of phospho-regulation. In the course of these studies we discovered a novel mechanism for loading protein phosphatase 2A (PP2A) onto AR. The loading mechanism requires small t antigen, a product encoded by SV40 that binds and alters the structure of a PP2A subunit. Current experiments are aimed at defining the structural basis of the PP2A loading reaction, as well as determining the cellular factors that mediate PP2A loading onto AR in untransformed cells.

    While biochemical analysis is the cornerstone of our nuclear transport and signal transduction studies, we also employ cell biological approaches including microinjection, fluorescence microscopy and real-time imaging in live cells, and animal models of tumorigenesis. Our studies benefit from ongoing collaborations with groups that specialize in mass spectrometry, pathology, and prostate cancer.


    Selected Publications
  • Shank, L.C. Kelley, J.B., Gioeli, D., Yang, C.Y., Spencer, A., Allison, L.A, and Paschal, B.M. (2008) Activation of the DNA-dependent protein kinase stimulates nuclear export of the androgen receptor in vitro. J. Biol. Chem., in press.
  • Yang CS, Xin HW, Kelley JB, Spencer A, Brautigan DL, Paschal BM. Ligand binding to the androgen receptor induces conformational changes that regulate phosphatase interactions. Mol Cell Biol. 2007 May;27(9):3390-404. Epub 2007 Feb 26.
  • Kesler, C. T., Gioeli, D., Conaway, MR, Weber, M., Paschal, B.M. (2007) Subcellular Localization Modulates AF-1 Domain Phosphorylation in the Androgen Receptor. Mol Endocrin. 21: 2071-2084.
  • Kelley, J.B. and Paschal, B.M. (2007) Hyperosmotic stress signaling to the nucleus disrupts the Ran gradient and the production of RanGTP. Mol Biol. Cell. 18: 4365-4376.
  • PubMed Listings for this Faculty Member

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    Contact Information
      Office Address: PO Box 800557, 
      Office Phone: +1 434-243-6521
      Home Phone: +1 434-964-1719

    Other Websites for this mentor:
    http://www.healthsystem.virginia.edu/internet/cellsignaling/bpaschal.cfm

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