Suppression of Huntington's disease pathology in Drosophila by human single-chain Fv antibodies.
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J. Marsh | L. Thompson | J. Huston | A. Messer | T. Miller | J. M. Webster | W. Wolfgang
[1] M. MacDonald,et al. A human single-chain Fv intrabody preferentially targets amino-terminal huntingtin fragments in striatal models of Huntington's disease , 2005, Neurobiology of Disease.
[2] Ann-Shyn Chiang,et al. Identification of combinatorial drug regimens for treatment of Huntington's disease using Drosophila. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[3] David W. Colby,et al. Potent inhibition of huntingtin aggregation and cytotoxicity by a disulfide bond-free single-domain intracellular antibody. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[4] M. Sierks,et al. A human single-chain Fv intrabody blocks aberrant cellular effects of overexpressed α-synuclein , 2004 .
[5] H. Voss,et al. Clinical protocol. Administration of a replication-deficient adeno-associated virus gene transfer vector expressing the human CLN2 cDNA to the brain of children with late infantile neuronal ceroid lipofuscinosis. , 2004, Human gene therapy.
[6] Mark R. Segal,et al. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death , 2004, Nature.
[7] R. Mandel,et al. Clinical trials in neurological disorders using AAV vectors: promises and challenges. , 2004, Current opinion in molecular therapeutics.
[8] K Dane Wittrup,et al. Development of a human light chain variable domain (V(L)) intracellular antibody specific for the amino terminus of huntingtin via yeast surface display. , 2004, Journal of molecular biology.
[9] T. Rabbitts,et al. Intracellular antibodies as specific reagents for functional ablation: future therapeutic molecules. , 2004, Current molecular medicine.
[10] G. Bates,et al. Progressive decrease in chaperone protein levels in a mouse model of Huntington's disease and induction of stress proteins as a therapeutic approach. , 2004, Human molecular genetics.
[11] C. Ross,et al. Protein aggregation and neurodegenerative disease , 2004, Nature Medicine.
[12] S. Lipton,et al. Molecular pathways to neurodegeneration , 2004, Nature Medicine.
[13] Francesco Scaravilli,et al. Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease , 2004, Nature Genetics.
[14] J. Marsh,et al. Can flies help humans treat neurodegenerative diseases? , 2004, BioEssays : news and reviews in molecular, cellular and developmental biology.
[15] M. Beal,et al. Experimental therapeutics in transgenic mouse models of Huntington's disease , 2004, Nature Reviews Neuroscience.
[16] R. Wetzel,et al. Inhibition of polyglutamine aggregate cytotoxicity by a structure‐based elongation inhibitor , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[17] J. Littleton,et al. Cytoplasmic aggregates trap polyglutamine-containing proteins and block axonal transport in a Drosophila model of Huntington's disease. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[18] Bin Yuan,et al. Inhibiting Aggregation of α-Synuclein with Human Single Chain Antibody Fragments† , 2004 .
[19] R. Murphy,et al. A single-chain Fv intrabody provides functional protection against the effects of mutant protein in an organotypic slice culture model of Huntington's disease. , 2004, Brain research. Molecular brain research.
[20] Nancy M Bonini,et al. Human neurodegenerative disease modeling using Drosophila. , 2003, Annual review of neuroscience.
[21] Leslie Michels Thompson,et al. A Rapid Cellular FRET Assay of Polyglutamine Aggregation Identifies a Novel Inhibitor , 2003, Neuron.
[22] Richard G. Brusch,et al. Disruption of Axonal Transport by Loss of Huntingtin or Expression of Pathogenic PolyQ Proteins in Drosophila , 2003, Neuron.
[23] D. Sane,et al. Intrabody and intrakine strategies for molecular therapy. , 2003, Molecular therapy : the journal of the American Society of Gene Therapy.
[24] W. Strittmatter,et al. Prevention of polyglutamine oligomerization and neurodegeneration by the peptide inhibitor QBP1 in Drosophila. , 2003, Human molecular genetics.
[25] James E Bear,et al. A cell-based assay for aggregation inhibitors as therapeutics of polyglutamine-repeat disease and validation in Drosophila , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[26] Carl W. Cotman,et al. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.
[27] Ari Helenius,et al. Quality control in the endoplasmic reticulum , 2003, Nature Reviews Molecular Cell Biology.
[28] Beate Gerstbrein,et al. Dying for a cause: invertebrate genetics takes on human neurodegeneration , 2003, Nature Reviews Genetics.
[29] Leslie M Thompson,et al. Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[30] H. Steven Wiley,et al. Flow-cytometric isolation of human antibodies from a nonimmune Saccharomyces cerevisiae surface display library , 2003, Nature Biotechnology.
[31] Junying Yuan,et al. Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders , 2003, Nature.
[32] Christopher A. Ross,et al. Huntingtin Spheroids and Protofibrils as Precursors in Polyglutamine Fibrilization* , 2002, The Journal of Biological Chemistry.
[33] H. Zoghbi,et al. Mouse and fly models of neurodegeneration. , 2002, Trends in genetics : TIG.
[34] T. Tabata,et al. Androgen-Dependent Neurodegeneration by Polyglutamine-Expanded Human Androgen Receptor in Drosophila , 2002, Neuron.
[35] D. Rubinsztein. Lessons from animal models of Huntington's disease. , 2002, Trends in genetics : TIG.
[36] D. Housman,et al. A bivalent Huntingtin binding peptide suppresses polyglutamine aggregation and pathogenesis in Drosophila , 2002, Nature Genetics.
[37] P. Patterson,et al. Effects of intracellular expression of anti-huntingtin antibodies of various specificities on mutant huntingtin aggregation and toxicity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[38] D. Housman,et al. Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila , 2001, Nature.
[39] D. Housman,et al. Human single-chain Fv intrabodies counteract in situ huntingtin aggregation in cellular models of Huntington's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[40] H. Zoghbi,et al. Identification of genes that modify ataxin-1-induced neurodegeneration , 2000, Nature.
[41] Martin R. Johnson,et al. A cancer gene therapy approach utilizing an anti-erbB-2 single-chain antibody-encoding adenovirus (AD21): a phase I trial. , 2000, Clinical cancer research : an official journal of the American Association for Cancer Research.
[42] S. Benzer,et al. Genetic suppression of polyglutamine toxicity in Drosophila. , 2000, Science.
[43] H. Paulson,et al. Suppression of polyglutamine-mediated neurodegeneration in Drosophila by the molecular chaperone HSP70 , 1999, Nature Genetics.
[44] Claire-Anne Gutekunst,et al. Nuclear and Neuropil Aggregates in Huntington’s Disease: Relationship to Neuropathology , 1999, The Journal of Neuroscience.
[45] Iris Salecker,et al. Polyglutamine-Expanded Human Huntingtin Transgenes Induce Degeneration of Drosophila Photoreceptor Neurons , 1998, Neuron.
[46] S. W. Davies,et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. , 1997, Science.
[47] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[48] S. W. Davies,et al. Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice , 1996, Cell.
[49] N. Perrimon,et al. Targeted gene expression as a means of altering cell fates and generating dominant phenotypes. , 1993, Development.
[50] Manish S. Shah,et al. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes , 1993, Cell.
[51] W. T. Catton. Information processing in the visual systems of arthropods , 1974 .
[52] K. N. Leibovic,et al. Information Processing in the Visual Systems of Arthropods , 1974 .
[53] F. Newell. Information Processing in the Visual Systems of Arthropods , 1973 .
[54] R. Murphy,et al. Gene transfer methods for CNS organotypic cultures: a comparison of three nonviral methods. , 2001, Molecular therapy : the journal of the American Society of Gene Therapy.
[55] H. Theisen,et al. Expanded polyglutamine peptides alone are intrinsically cytotoxic and cause neurodegeneration in Drosophila. , 2000, Human molecular genetics.
[56] A. Cossins,et al. Responses of the Na+/H+ exchanger of European flounder red blood cells to hypertonic, beta-adrenergic and acidotic stimuli. , 1999, The Journal of experimental biology.
[57] E. Haber,et al. Antibody binding sites. , 1996, Advances in protein chemistry.