Roger F Duncan

Summary

Affiliation: University of Southern California
Country: USA

Publications

  1. ncbi request reprint Signal transduction pathways leading to increased eIF4E phosphorylation caused by oxidative stress
    Roger F Duncan
    Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90033, USA
    Free Radic Biol Med 38:631-43. 2005
  2. ncbi request reprint Inhibition of Hsp90 function delays and impairs recovery from heat shock
    Roger F Duncan
    Department of Molecular Pharmacology and Toxicology, University of Southern California School of Pharmacy, Los Angeles, CA, USA
    FEBS J 272:5244-56. 2005
  3. pmc Rapamycin conditionally inhibits Hsp90 but not Hsp70 mRNA translation in Drosophila: implications for the mechanisms of Hsp mRNA translation
    Roger F Duncan
    Department of Pharmacology and Pharmaceutical Sciences, University of Southern California School of Pharmacy, 1985 Zonal Avenue, Los Angeles, CA 90033, USA
    Cell Stress Chaperones 13:143-55. 2008
  4. ncbi request reprint Translational regulation of Hsp90 mRNA. AUG-proximal 5'-untranslated region elements essential for preferential heat shock translation
    Ruhi Ahmed
    University of Southern California School of Pharmacy, Department of Molecular Pharmacology and Toxicology and School of Medicine, Los Angeles, California 90033, USA
    J Biol Chem 279:49919-30. 2004
  5. pmc Oxidative stress increases eukaryotic initiation factor 4E phosphorylation in vascular cells
    Roger F Duncan
    Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90033, U S A
    Biochem J 369:213-25. 2003
  6. pmc c-Jun N-terminal kinase (JNK)-mediated modulation of brain mitochondria function: new target proteins for JNK signalling in mitochondrion-dependent apoptosis
    Hagen Schroeter
    Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles 90089 9121, USA
    Biochem J 372:359-69. 2003
  7. ncbi request reprint Hepatitis C virus IRES-dependent translation is insensitive to an eIF2alpha-independent mechanism of inhibition by interferon in hepatocyte cell lines
    Gennadiy Koev
    Howard Hughes Medical Institute, Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA
    Virology 297:195-202. 2002

Collaborators

Detail Information

Publications7

  1. ncbi request reprint Signal transduction pathways leading to increased eIF4E phosphorylation caused by oxidative stress
    Roger F Duncan
    Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90033, USA
    Free Radic Biol Med 38:631-43. 2005
    ....
  2. ncbi request reprint Inhibition of Hsp90 function delays and impairs recovery from heat shock
    Roger F Duncan
    Department of Molecular Pharmacology and Toxicology, University of Southern California School of Pharmacy, Los Angeles, CA, USA
    FEBS J 272:5244-56. 2005
    ..Impaired function of either component is sufficient to alter the heat shock response...
  3. pmc Rapamycin conditionally inhibits Hsp90 but not Hsp70 mRNA translation in Drosophila: implications for the mechanisms of Hsp mRNA translation
    Roger F Duncan
    Department of Pharmacology and Pharmaceutical Sciences, University of Southern California School of Pharmacy, 1985 Zonal Avenue, Los Angeles, CA 90033, USA
    Cell Stress Chaperones 13:143-55. 2008
    ..These results support the proposal that preferential translation of different Hsp mRNA utilizes distinct translation mechanisms, even within a single species...
  4. ncbi request reprint Translational regulation of Hsp90 mRNA. AUG-proximal 5'-untranslated region elements essential for preferential heat shock translation
    Ruhi Ahmed
    University of Southern California School of Pharmacy, Department of Molecular Pharmacology and Toxicology and School of Medicine, Los Angeles, California 90033, USA
    J Biol Chem 279:49919-30. 2004
    ..We present a model to account for Hsp90 mRNA translation, incorporating results indicating that heat shock inhibits eIF4F activity, and that Hsp90 mRNA translation is sensitive to eIF4F inactivation...
  5. pmc Oxidative stress increases eukaryotic initiation factor 4E phosphorylation in vascular cells
    Roger F Duncan
    Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90033, U S A
    Biochem J 369:213-25. 2003
    ..The results of this study indicate that increased eIF4E activity may contribute to the pathophysiological events in early atherogenesis by increasing the expression of translationally inefficient mRNAs encoding growth-promoting proteins...
  6. pmc c-Jun N-terminal kinase (JNK)-mediated modulation of brain mitochondria function: new target proteins for JNK signalling in mitochondrion-dependent apoptosis
    Hagen Schroeter
    Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles 90089 9121, USA
    Biochem J 372:359-69. 2003
    ..Taken together, JNK-dependent phosphorylation of mitochondrial proteins including, but not limited to, Bcl-2/Bcl-x(L) may represent a potential of the modulation of mitochondrial function during apoptosis...
  7. ncbi request reprint Hepatitis C virus IRES-dependent translation is insensitive to an eIF2alpha-independent mechanism of inhibition by interferon in hepatocyte cell lines
    Gennadiy Koev
    Howard Hughes Medical Institute, Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA
    Virology 297:195-202. 2002
    ..This may present a new potential mechanism of viral resistance to IFN treatment during the early steps of virus infection...