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Jaquelin P Dudley
Professor, Professor of Oncology
Molecular Biosciences, Department of OncologyMolecular biology and pathogenesis of retrovirusesjdudley@austin.utexas.edu
Phone: 512-471-8415
Office Location
NMS 2.122
Postal Address
2506 SPEEDWAY
AUSTIN, TX 78712-
1973-78 Graduate student with Dr. Janet Butel, Baylor College of Medicine, Houston, TX 1978-80 Postdoctoral fellow with Nobel laureate Harold Varmus, University of California, San Francisco, CA 1980-82 Postdoctoral fellow with Dr. Rex Risser, McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI 1983-89 Assistant Professor, Dept. of Microbiology, University of Texas at Austin, Austin, TX 1989-96
Associate Professor, Dept. of Microbiology, University of Texas at Austin, Austin, TX
1991-03 Member, Board of Directors, Gala Industries, Inc.
1996- Professor, Dept. of Microbiology, University of Texas at Austin, Austin, TX
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Research Summary:
Mouse mammary tumor virus (MMTV) is a retrovirus that induces mammary carcinomas and T-cell lymphomas in mice by insertional mutagenesis. We recently discovered a novel viral protein, Rem, which is involved in the nuclear export and expression of intron-containing viral mRNAs. These results are exciting because MMTV serves as a mouse model for study of another retrovirus, human immunodeficiency virus (HIV), which causes AIDS. Our recent results suggest that Rem has a very unusual trafficking pattern within mammalian cells. Prior to nuclear entry, Rem appears to enter the endoplasmic reticulum (ER), where it is partially glycosylated, and cleaved by signal peptidase. Cleavage appears to yield an HIV Rev-like gene product, SP, as well as a unique product (Rem-CT) of unknown function. Mutations that prevent the correct processing and glycosylation of Rem interfere with SP activity in reporter assays. Rem trafficking through the ER is required for Rem processing and function in the nucleus after signal peptidase cleavage and retrotranslocation of the N-terminal SP out of the ER. Retrotranslocation is associated with endoplasmic reticulum-associated degradation (ERAD). ERAD is a poorly understood cellular process that is responsible for disposal of misfolded proteins. Numerous human diseases, including cancer and neurogeneration, show defects in ERAD. Recent exciting data indicate that the Rem C-terminus has a separate function in intrinsic immunity. Finally, we are in the process of developing vectors for gene therapy of breast cancer. Our studies have allowed the extensive mapping of the MMTV genome, which has been evolutionarily selected for optimal expression in the mammary gland. Elimination of viral genes, introduction of reporter genes, and manipulation of tissue-specific promoter elements should enable us to develop and test new vectors for safety and efficacy in mice. Our goal is to provide more specific and less toxic treatments for human breast cancer.
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1984
Selected for inclusion in the 1984 Esquire Magazine Register of "Outstanding Americans Under Age 40"
2006
Recipient of the Ohio State University Center for Retrovirus Research Distinguished Research Career Award 2006
Co-organizer of the Cold Spring Meeting on Retroviruses 2006
Co-organizer of the West Coast Retrovirus Meeting 2007-present
Editorial Board, Journal of Virology 2007-present
Editorial Board, The Open Virology Journal 2007
Molecular Genetics and Microbiology Teaching Excellence Award 2007
College of Natural Sciences Teaching Excellence Award 2008-present
Editorial Board, Advances in Virology 2009
Elected Fellow, American Academy of Microbiology 2010-present
Editorial Board, Virology
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Advanced Virology (BIO391P)
Animal Virology (BIO330)
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Training for both graduate and undergraduate students is available.
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