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Journal Abstract Search

457 related items for PubMed ID: 25568955

  • 1. Heterologous aggregates promote de novo prion appearance via more than one mechanism.
    Arslan F, Hong JY, Kanneganti V, Park SK, Liebman SW.
    PLoS Genet; 2015 Jan; 11(1):e1004814. PubMed ID: 25568955
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  • 8. Heterologous gln/asn-rich proteins impede the propagation of yeast prions by altering chaperone availability.
    Yang Z, Hong JY, Derkatch IL, Liebman SW.
    PLoS Genet; 2013 Jan; 9(1):e1003236. PubMed ID: 23358669
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  • 9. The relationship between visible intracellular aggregates that appear after overexpression of Sup35 and the yeast prion-like elements [PSI(+)] and [PIN(+)].
    Zhou P, Derkatch IL, Liebman SW.
    Mol Microbiol; 2001 Jan; 39(1):37-46. PubMed ID: 11123686
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  • 10. Pathogenic polyglutamine tracts are potent inducers of spontaneous Sup35 and Rnq1 amyloidogenesis.
    Goehler H, Dröge A, Lurz R, Schnoegl S, Chernoff YO, Wanker EE.
    PLoS One; 2010 Mar 10; 5(3):e9642. PubMed ID: 20224794
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  • 12. Exploring the basis of [PIN(+)] variant differences in [PSI(+)] induction.
    Sharma J, Liebman SW.
    J Mol Biol; 2013 Sep 09; 425(17):3046-59. PubMed ID: 23770111
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  • 13. [PSI(+)] aggregate enlargement in rnq1 nonprion domain mutants, leading to a loss of prion in yeast.
    Kurahashi H, Pack CG, Shibata S, Oishi K, Sako Y, Nakamura Y.
    Genes Cells; 2011 May 09; 16(5):576-89. PubMed ID: 21453425
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  • 16. A regulatory role of the Rnq1 nonprion domain for prion propagation and polyglutamine aggregates.
    Kurahashi H, Ishiwata M, Shibata S, Nakamura Y.
    Mol Cell Biol; 2008 May 09; 28(10):3313-23. PubMed ID: 18332119
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  • 20. Prions affect the appearance of other prions: the story of [PIN(+)].
    Derkatch IL, Bradley ME, Hong JY, Liebman SW.
    Cell; 2001 Jul 27; 106(2):171-82. PubMed ID: 11511345
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