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775 related items for PubMed ID: 26071686

  • 1. Autophagy and UPR in alpha-crystallin mutant knock-in mouse models of hereditary cataracts.
    Andley UP, Goldman JW.
    Biochim Biophys Acta; 2016 Jan; 1860(1 Pt B):234-9. PubMed ID: 26071686
    [Abstract] [Full Text] [Related]

  • 2. p62 expression and autophagy in αB-crystallin R120G mutant knock-in mouse model of hereditary cataract.
    Wignes JA, Goldman JW, Weihl CC, Bartley MG, Andley UP.
    Exp Eye Res; 2013 Oct; 115():263-73. PubMed ID: 23872361
    [Abstract] [Full Text] [Related]

  • 3. Mechanism of small heat shock protein function in vivo: a knock-in mouse model demonstrates that the R49C mutation in alpha A-crystallin enhances protein insolubility and cell death.
    Xi JH, Bai F, Gross J, Townsend RR, Menko AS, Andley UP.
    J Biol Chem; 2008 Feb 29; 283(9):5801-14. PubMed ID: 18056999
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  • 4. Probing the changes in gene expression due to α-crystallin mutations in mouse models of hereditary human cataract.
    Andley UP, Tycksen E, McGlasson-Naumann BN, Hamilton PD.
    PLoS One; 2018 Feb 29; 13(1):e0190817. PubMed ID: 29338044
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  • 5. Changes in relative histone abundance and heterochromatin in αA-crystallin and αB-crystallin knock-in mutant mouse lenses.
    Andley UP, Naumann BN, Hamilton PD, Bozeman SL.
    BMC Res Notes; 2020 Jul 02; 13(1):315. PubMed ID: 32616056
    [Abstract] [Full Text] [Related]

  • 6. Activation of the unfolded protein response by a cataract-associated αA-crystallin mutation.
    Watson GW, Andley UP.
    Biochem Biophys Res Commun; 2010 Oct 15; 401(2):192-6. PubMed ID: 20833134
    [Abstract] [Full Text] [Related]

  • 7. In vivo substrates of the lens molecular chaperones αA-crystallin and αB-crystallin.
    Andley UP, Malone JP, Townsend RR.
    PLoS One; 2014 Oct 15; 9(4):e95507. PubMed ID: 24760011
    [Abstract] [Full Text] [Related]

  • 8. In vivo lens deficiency of the R49C alphaA-crystallin mutant.
    Andley UP, Reilly MA.
    Exp Eye Res; 2010 Jun 15; 90(6):699-702. PubMed ID: 20188090
    [Abstract] [Full Text] [Related]

  • 9. Mechanism of insolubilization by a single-point mutation in alphaA-crystallin linked with hereditary human cataracts.
    Andley UP, Hamilton PD, Ravi N.
    Biochemistry; 2008 Sep 09; 47(36):9697-706. PubMed ID: 18700785
    [Abstract] [Full Text] [Related]

  • 10. AlphaA-crystallin R49Cneo mutation influences the architecture of lens fiber cell membranes and causes posterior and nuclear cataracts in mice.
    Andley UP.
    BMC Ophthalmol; 2009 Jul 20; 9():4. PubMed ID: 19619312
    [Abstract] [Full Text] [Related]

  • 11. Analysis of amyloid-like secondary structure in the Cryab-R120G knock-in mouse model of hereditary cataracts by two-dimensional infrared spectroscopy.
    Alperstein AM, Molnar KS, Dicke SS, Farrell KM, Makley LN, Zanni MT, Andley UP.
    PLoS One; 2021 Jul 20; 16(9):e0257098. PubMed ID: 34520490
    [Abstract] [Full Text] [Related]

  • 12. Arginine 54 and Tyrosine 118 residues of {alpha}A-crystallin are crucial for lens formation and transparency.
    Xia CH, Liu H, Chang B, Cheng C, Cheung D, Wang M, Huang Q, Horwitz J, Gong X.
    Invest Ophthalmol Vis Sci; 2006 Jul 20; 47(7):3004-10. PubMed ID: 16799046
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  • 16. Human βA3/A1-crystallin splicing mutation causes cataracts by activating the unfolded protein response and inducing apoptosis in differentiating lens fiber cells.
    Ma Z, Yao W, Chan CC, Kannabiran C, Wawrousek E, Hejtmancik JF.
    Biochim Biophys Acta; 2016 Jun 20; 1862(6):1214-27. PubMed ID: 26851658
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