These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


BIOMARKERS

Molecular Biopsy of Human Tumors

- a resource for Precision Medicine *

133 related articles for article (PubMed ID: 10797551)

  • 1. Polyglutamine-induced ion channels: a possible mechanism for the neurotoxicity of Huntington and other CAG repeat diseases.
    Hirakura Y; Azimov R; Azimova R; Kagan BL
    J Neurosci Res; 2000 May; 60(4):490-4. PubMed ID: 10797551
    [TBL] [Abstract][Full Text] [Related]  

  • 2. Poly-L-glutamine forms cation channels: relevance to the pathogenesis of the polyglutamine diseases.
    Monoi H; Futaki S; Kugimiya S; Minakata H; Yoshihara K
    Biophys J; 2000 Jun; 78(6):2892-9. PubMed ID: 10827970
    [TBL] [Abstract][Full Text] [Related]  

  • 3. Cells exposed to a huntingtin fragment containing an expanded polyglutamine tract show no sign of ion channel formation: results arguing against the ion channel hypothesis.
    Nørremølle A; Grunnet M; Hasholt L; Sørensen SA
    J Neurosci Res; 2003 Jan; 71(1):132-7. PubMed ID: 12478622
    [TBL] [Abstract][Full Text] [Related]  

  • 4. Preparation of human cDNas encoding expanded polyglutamine repeats.
    Peters MF; Ross CA
    Neurosci Lett; 1999 Nov; 275(2):129-32. PubMed ID: 10568516
    [TBL] [Abstract][Full Text] [Related]  

  • 5. The channel hypothesis of Huntington's disease.
    Kagan BL; Hirakura Y; Azimov R; Azimova R
    Brain Res Bull; 2001 Oct-Nov 1; 56(3-4):281-4. PubMed ID: 11719262
    [TBL] [Abstract][Full Text] [Related]  

  • 6. Lysine-rich histone (H1) is a lysyl substrate of tissue transglutaminase: possible involvement of transglutaminase in the formation of nuclear aggregates in (CAG)(n)/Q(n) expansion diseases.
    Cooper AJ; Wang J; Pasternack R; Fuchsbauer HL; Sheu RK; Blass JP
    Dev Neurosci; 2000; 22(5-6):404-17. PubMed ID: 11111157
    [TBL] [Abstract][Full Text] [Related]  

  • 7. The CAG-polyglutamine repeat diseases: a clinical, molecular, genetic, and pathophysiologic nosology.
    Stoyas CA; La Spada AR
    Handb Clin Neurol; 2018; 147():143-170. PubMed ID: 29325609
    [TBL] [Abstract][Full Text] [Related]  

  • 8. Giant multilevel cation channels formed by Alzheimer disease amyloid beta-protein [A beta P-(1-40)] in bilayer membranes.
    Arispe N; Pollard HB; Rojas E
    Proc Natl Acad Sci U S A; 1993 Nov; 90(22):10573-7. PubMed ID: 7504270
    [TBL] [Abstract][Full Text] [Related]  

  • 9. Membrane channel formation by antimicrobial protegrins.
    Sokolov Y; Mirzabekov T; Martin DW; Lehrer RI; Kagan BL
    Biochim Biophys Acta; 1999 Aug; 1420(1-2):23-9. PubMed ID: 10446287
    [TBL] [Abstract][Full Text] [Related]  

  • 10. Age-, tissue- and length-dependent bidirectional somatic CAG•CTG repeat instability in an allelic series of R6/2 Huntington disease mice.
    Larson E; Fyfe I; Morton AJ; Monckton DG
    Neurobiol Dis; 2015 Apr; 76():98-111. PubMed ID: 25662336
    [TBL] [Abstract][Full Text] [Related]  

  • 11. Heterogeneous amyloid-formed ion channels as a common cytotoxic mechanism: implications for therapeutic strategies against amyloidosis.
    Kourie JI; Culverson AL; Farrelly PV; Henry CL; Laohachai KN
    Cell Biochem Biophys; 2002; 36(2-3):191-207. PubMed ID: 12139405
    [TBL] [Abstract][Full Text] [Related]  

  • 12. Polyglutamine expansion neurodegenerative disease.
    Fischbeck KH
    Brain Res Bull; 2001 Oct-Nov 1; 56(3-4):161-3. PubMed ID: 11719245
    [TBL] [Abstract][Full Text] [Related]  

  • 13. [Huntington's disease: trinucleotide disease or polyglutamine disease?].
    Ide K; Nukina N; Kanazawa I
    Rinsho Shinkeigaku; 1995 Dec; 35(12):1540-1. PubMed ID: 8752457
    [TBL] [Abstract][Full Text] [Related]  

  • 14. Pathogenesis of polyglutamine disorders: aggregation revisited.
    Michalik A; Van Broeckhoven C
    Hum Mol Genet; 2003 Oct; 12 Spec No 2():R173-86. PubMed ID: 14504263
    [TBL] [Abstract][Full Text] [Related]  

  • 15. Abundant expression and cytoplasmic aggregations of [alpha]1A voltage-dependent calcium channel protein associated with neurodegeneration in spinocerebellar ataxia type 6.
    Ishikawa K; Fujigasaki H; Saegusa H; Ohwada K; Fujita T; Iwamoto H; Komatsuzaki Y; Toru S; Toriyama H; Watanabe M; Ohkoshi N; Shoji S; Kanazawa I; Tanabe T; Mizusawa H
    Hum Mol Genet; 1999 Jul; 8(7):1185-93. PubMed ID: 10369863
    [TBL] [Abstract][Full Text] [Related]  

  • 16. New cationic lipids form channel-like pores in phospholipid bilayers.
    Chanturiya A; Yang J; Scaria P; Stanek J; Frei J; Mett H; Woodle M
    Biophys J; 2003 Mar; 84(3):1750-5. PubMed ID: 12609876
    [TBL] [Abstract][Full Text] [Related]  

  • 17. Extended polyglutamine selectively interacts with caspase-8 and -10 in nuclear aggregates.
    U M; Miyashita T; Ohtsuka Y; Okamura-Oho Y; Shikama Y; Yamada M
    Cell Death Differ; 2001 Apr; 8(4):377-86. PubMed ID: 11550089
    [TBL] [Abstract][Full Text] [Related]  

  • 18. The unstable trinucleotide repeat story of major psychosis.
    Vincent JB; Paterson AD; Strong E; Petronis A; Kennedy JL
    Am J Med Genet; 2000; 97(1):77-97. PubMed ID: 10813808
    [TBL] [Abstract][Full Text] [Related]  

  • 19. Late-onset Huntington disease with intermediate CAG repeats: true or false?
    Groen JL; de Bie RM; Foncke EM; Roos RA; Leenders KL; Tijssen MA
    J Neurol Neurosurg Psychiatry; 2010 Feb; 81(2):228-30. PubMed ID: 20145031
    [TBL] [Abstract][Full Text] [Related]  

  • 20. Amyloid formation by mutant huntingtin: threshold, progressivity and recruitment of normal polyglutamine proteins.
    Huang CC; Faber PW; Persichetti F; Mittal V; Vonsattel JP; MacDonald ME; Gusella JF
    Somat Cell Mol Genet; 1998 Jul; 24(4):217-33. PubMed ID: 10410676
    [TBL] [Abstract][Full Text] [Related]  

    [Next]    [New Search]
    of 7.