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Journal Abstract Search

215 related items for PubMed ID: 15760896

  • 1. Degradation of trafficking-defective long QT syndrome type II mutant channels by the ubiquitin-proteasome pathway.
    Gong Q, Keeney DR, Molinari M, Zhou Z.
    J Biol Chem; 2005 May 13; 280(19):19419-25. PubMed ID: 15760896
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  • 4. Trafficking-deficient hERG K⁺ channels linked to long QT syndrome are regulated by a microtubule-dependent quality control compartment in the ER.
    Smith JL, McBride CM, Nataraj PS, Bartos DC, January CT, Delisle BP.
    Am J Physiol Cell Physiol; 2011 Jul 13; 301(1):C75-85. PubMed ID: 21490315
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  • 8. Hsp40 chaperones promote degradation of the HERG potassium channel.
    Walker VE, Wong MJ, Atanasiu R, Hantouche C, Young JC, Shrier A.
    J Biol Chem; 2010 Jan 29; 285(5):3319-29. PubMed ID: 19940115
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  • 9. Pharmacological rescue of trafficking defective HERG channels formed by coassembly of wild-type and long QT mutant N470D subunits.
    Gong Q, Anderson CL, January CT, Zhou Z.
    Am J Physiol Heart Circ Physiol; 2004 Aug 29; 287(2):H652-8. PubMed ID: 15072950
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  • 12. Degradation of the sodium taurocholate cotransporting polypeptide (NTCP) by the ubiquitin-proteasome system.
    Kühlkamp T, Keitel V, Helmer A, Häussinger D, Kubitz R.
    Biol Chem; 2005 Oct 29; 386(10):1065-74. PubMed ID: 16218878
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  • 14. The met receptor degradation pathway: requirement for Lys48-linked polyubiquitin independent of proteasome activity.
    Carter S, Urbé S, Clague MJ.
    J Biol Chem; 2004 Dec 17; 279(51):52835-9. PubMed ID: 15466866
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  • 16. Gradually glycosylated protein C mutants (Arg178Gln and Cys331Arg) are degraded by proteasome after mannose trimming.
    Nakahara M, Koyama T, Nakazawa F, Nishio M, Shibamiya A, Hirosawa S.
    Thromb Haemost; 2004 Dec 17; 92(6):1284-90. PubMed ID: 15583735
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  • 17. Growth-associated protein-43 is degraded via the ubiquitin-proteasome system.
    De Moliner KL, Wolfson ML, Perrone Bizzozero N, Adamo AM.
    J Neurosci Res; 2005 Mar 01; 79(5):652-60. PubMed ID: 15668958
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  • 18. Retention in the endoplasmic reticulum as a mechanism of dominant-negative current suppression in human long QT syndrome.
    Ficker E, Dennis AT, Obejero-Paz CA, Castaldo P, Taglialatela M, Brown AM.
    J Mol Cell Cardiol; 2000 Dec 01; 32(12):2327-37. PubMed ID: 11113008
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