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Journal Abstract Search

257 related items for PubMed ID: 20414249

  • 1. Imbalances in p97 co-factor interactions in human proteinopathy.
    Fernández-Sáiz V, Buchberger A.
    EMBO Rep; 2010 Jun; 11(6):479-85. PubMed ID: 20414249
    [Abstract] [Full Text] [Related]

  • 2. A unique IBMPFD-related P97/VCP mutation with differential binding pattern and subcellular localization.
    Erzurumlu Y, Kose FA, Gozen O, Gozuacik D, Toth EA, Ballar P.
    Int J Biochem Cell Biol; 2013 Apr; 45(4):773-82. PubMed ID: 23333620
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  • 3. Structural and functional deviations in disease-associated p97 mutants.
    Tang WK, Xia D.
    J Struct Biol; 2012 Aug; 179(2):83-92. PubMed ID: 22579784
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  • 4. Inclusion body myopathy, Paget's disease of the bone and fronto-temporal dementia: a disorder of autophagy.
    Ju JS, Weihl CC.
    Hum Mol Genet; 2010 Apr 15; 19(R1):R38-45. PubMed ID: 20410287
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  • 6. Transgenic mice expressing mutant forms VCP/p97 recapitulate the full spectrum of IBMPFD including degeneration in muscle, brain and bone.
    Custer SK, Neumann M, Lu H, Wright AC, Taylor JP.
    Hum Mol Genet; 2010 May 01; 19(9):1741-55. PubMed ID: 20147319
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  • 7. Inclusion body myopathy-associated mutations in p97/VCP impair endoplasmic reticulum-associated degradation.
    Weihl CC, Dalal S, Pestronk A, Hanson PI.
    Hum Mol Genet; 2006 Jan 15; 15(2):189-99. PubMed ID: 16321991
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  • 8. Ubiquitin- and ATP-dependent unfoldase activity of P97/VCP•NPLOC4•UFD1L is enhanced by a mutation that causes multisystem proteinopathy.
    Blythe EE, Olson KC, Chau V, Deshaies RJ.
    Proc Natl Acad Sci U S A; 2017 May 30; 114(22):E4380-E4388. PubMed ID: 28512218
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  • 9. Pathogenic VCP/TER94 alleles are dominant actives and contribute to neurodegeneration by altering cellular ATP level in a Drosophila IBMPFD model.
    Chang YC, Hung WT, Chang YC, Chang HC, Wu CL, Chiang AS, Jackson GR, Sang TK.
    PLoS Genet; 2011 Feb 03; 7(2):e1001288. PubMed ID: 21304887
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  • 10. Enhanced ATPase activities as a primary defect of mutant valosin-containing proteins that cause inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia.
    Manno A, Noguchi M, Fukushi J, Motohashi Y, Kakizuka A.
    Genes Cells; 2010 Aug 03; 15(8):911-22. PubMed ID: 20604808
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  • 12. VCP/p97 is essential for maturation of ubiquitin-containing autophagosomes and this function is impaired by mutations that cause IBMPFD.
    Tresse E, Salomons FA, Vesa J, Bott LC, Kimonis V, Yao TP, Dantuma NP, Taylor JP.
    Autophagy; 2010 Feb 03; 6(2):217-27. PubMed ID: 20104022
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  • 13. Phenotypic variability in three families with valosin-containing protein mutation.
    Spina S, Van Laar AD, Murrell JR, Hamilton RL, Kofler JK, Epperson F, Farlow MR, Lopez OL, Quinlan J, DeKosky ST, Ghetti B.
    Eur J Neurol; 2013 Feb 03; 20(2):251-8. PubMed ID: 22900631
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  • 16. Altered intersubunit communication is the molecular basis for functional defects of pathogenic p97 mutants.
    Tang WK, Xia D.
    J Biol Chem; 2013 Dec 20; 288(51):36624-35. PubMed ID: 24196964
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  • 17. Neuronal-specific overexpression of a mutant valosin-containing protein associated with IBMPFD promotes aberrant ubiquitin and TDP-43 accumulation and cognitive dysfunction in transgenic mice.
    Rodriguez-Ortiz CJ, Hoshino H, Cheng D, Liu-Yescevitz L, Blurton-Jones M, Wolozin B, LaFerla FM, Kitazawa M.
    Am J Pathol; 2013 Aug 20; 183(2):504-15. PubMed ID: 23747512
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  • 20. Transgenic expression of inclusion body myopathy associated mutant p97/VCP causes weakness and ubiquitinated protein inclusions in mice.
    Weihl CC, Miller SE, Hanson PI, Pestronk A.
    Hum Mol Genet; 2007 Apr 15; 16(8):919-28. PubMed ID: 17329348
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