Lentiviral-Mediated Delivery of Mutant Huntingtin in the Striatum of Rats Induces a Selective Neuropathology Modulated by Polyglutamine Repeat Size, Huntingtin Expression Levels, and Protein Length
暂无分享,去创建一个
Christopher A. Ross | Patrick Aebischer | C. Ross | N. Déglon | P. Aebischer | D. Zala | Diana Zala | Luis Pereira de Almeida | Nicole Déglon | L. P. de Almeida
[1] A. Hackam,et al. Length of huntingtin and its polyglutamine tract influences localization and frequency of intracellular aggregates , 1998, Nature Genetics.
[2] G P Bates,et al. Ultrastructural localization and progressive formation of neuropil aggregates in Huntington's disease transgenic mice. , 1999, Human molecular genetics.
[3] Fumiaki Tanaka,et al. Nuclear inclusions of the androgen receptor protein in spinal and bulbar muscular atrophy , 1998, Annals of neurology.
[4] N. Déglon,et al. Neuroprotective Effect of a CNTF-Expressing Lentiviral Vector in the Quinolinic Acid Rat Model of Huntington's Disease , 2001, Neurobiology of Disease.
[5] P. Harper,et al. Localization of rabbit huntingtin using a new panel of monoclonal antibodies. , 1999, Brain research. Molecular brain research.
[6] Intranuclear inclusions in subtypes of striatal neurons in Huntington's disease transgenic mice. , 1999, Neuroreport.
[7] Joseph B. Martin,et al. Sparing of acetylcholinesterase-containing striatal neurons in Huntington's disease , 1987, Brain Research.
[8] D. Borchelt,et al. Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin. , 1999, Human molecular genetics.
[9] D. Craufurd,et al. Mutation size and age at onset in Huntington's disease. , 1993, Journal of medical genetics.
[10] Joseph B. Martin,et al. Subset of neurons characterized by the presence of NADPH‐diaphorase in human substantia innominata , 1987, The Journal of comparative neurology.
[11] René Hen,et al. Reversal of Neuropathology and Motor Dysfunction in a Conditional Model of Huntington's Disease , 2000, Cell.
[12] Paul Greengard,et al. Quantitative immunocytochemistry of DARPP-32-expressing neurons in the rat caudatoputamen , 1998, Brain Research.
[13] R N Gunn,et al. Huntington's disease progression. PET and clinical observations. , 1999, Brain : a journal of neurology.
[14] S. Sisodia. Nuclear Inclusions in Glutamine Repeat Disorders Are They Pernicious, Coincidental, or Beneficial? , 1998, Cell.
[15] D. Tagle,et al. Mutant Huntingtin Expression in Clonal Striatal Cells: Dissociation of Inclusion Formation and Neuronal Survival by Caspase Inhibition , 1999, The Journal of Neuroscience.
[16] J. Penney,et al. Trinucleotide repeat length instability and age of onset in Huntington's disease , 1993, Nature Genetics.
[17] S. Hersch,et al. Huntingtin aggregates may not predict neuronal death in Huntington's disease , 1999 .
[18] Claire-Anne Gutekunst,et al. A YAC Mouse Model for Huntington’s Disease with Full-Length Mutant Huntingtin, Cytoplasmic Toxicity, and Selective Striatal Neurodegeneration , 1999, Neuron.
[19] L. Naldini. Lentiviruses as gene transfer agents for delivery to non-dividing cells. , 1998, Current opinion in biotechnology.
[20] M. MacDonald,et al. Relationship between trinucleotide repeat expansion and phenotypic variation in Huntington's disease , 1993, Nature Genetics.
[21] J. Schulz,et al. High level expression of expanded full-length ataxin-3 in vitro causes cell death and formation of intranuclear inclusions in neuronal cells. , 1999, Human molecular genetics.
[22] S. W. Davies,et al. Intranuclear Neuronal Inclusions in Huntington's Disease and Dentatorubral and Pallidoluysian Atrophy: Correlation between the Density of Inclusions andIT15CAG Triplet Repeat Length , 1998, Neurobiology of Disease.
[23] S. Suhr,et al. Intraneuronal Aggregate Formation and Cell Death after Viral Expression of Expanded Polyglutamine Tracts in the Adult Rat Brain , 2000, The Journal of Neuroscience.
[24] Jacqueline K. White,et al. Huntingtin is required for neurogenesis and is not impaired by the Huntington's disease CAG expansion , 1997, Nature Genetics.
[25] T. Uchihara,et al. Neuronal intranuclear inclusions in spinocerebellar ataxia type 2: triple-labeling immunofluorescent study , 1999, Neuroscience Letters.
[26] S. W. Davies,et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. , 1997, Science.
[27] C A Ross,et al. Truncated N-terminal fragments of huntingtin with expanded glutamine repeats form nuclear and cytoplasmic aggregates in cell culture. , 1998, Human molecular genetics.
[28] M. Hayden,et al. The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington's disease , 1993, Nature Genetics.
[29] Y. Arsenijévic,et al. Self-inactivating lentiviral vectors with enhanced transgene expression as potential gene transfer system in Parkinson's disease. , 2000, Human gene therapy.
[30] He Li,et al. Amino-terminal fragments of mutant huntingtin show selective accumulation in striatal neurons and synaptic toxicity , 2000, Nature Genetics.
[31] R H Myers,et al. Quantitative neuropathological changes in presymptomatic Huntington's disease , 2001, Annals of neurology.
[32] P. Greengard,et al. Severe deficiencies in dopamine signaling in presymptomatic Huntington's disease mice. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[33] A. Morton,et al. Dopamine Modulates the Susceptibility of Striatal Neurons to 3-Nitropropionic Acid in the Rat Model of Huntington’s Disease , 1998, The Journal of Neuroscience.
[34] Scott T. Grafton,et al. A comparison of neurological, metabolic, structural, and genetic evaluations in persons at risk for Huntington's disease , 1990, Annals of neurology.
[35] M. MacDonald,et al. Normal and Expanded Huntington’s Disease Gene Alleles Produce Distinguishable Proteins Due to Translation Across the CAG Repeat , 1995, Molecular medicine.
[36] P Boesiger,et al. Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington's disease. , 1996, Brain : a journal of neurology.
[37] D. Borchelt,et al. Distinct Behavioral and Neuropathological Abnormalities in Transgenic Mouse Models of HD and DRPLA , 2001, Neurobiology of Disease.
[38] 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.
[39] Steven Finkbeiner,et al. Huntingtin Acts in the Nucleus to Induce Apoptosis but Death Does Not Correlate with the Formation of Intranuclear Inclusions , 1998, Cell.
[40] A. Hackam,et al. Wild-Type Huntingtin Protects from Apoptosis Upstream of Caspase-3 , 2000, The Journal of Neuroscience.
[41] D. Tagle,et al. Transgenic mice expressing mutated full-length HD cDNA: a paradigm for locomotor changes and selective neuronal loss in Huntington's disease. , 1999, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.
[42] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[43] F. Gage,et al. In Vivo Gene Delivery and Stable Transduction of Nondividing Cells by a Lentiviral Vector , 1996, Science.
[44] O. Suchowersky,et al. Relationship between trinucliotide repeats and neuropathological changes in Huntington's diease , 1996, Annals of neurology.
[45] Lisa Garrett,et al. Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA , 1998, Nature Genetics.
[46] D. Tagle,et al. Recent advances in understanding the pathogenesis of Huntington's disease , 1999, Trends in Neurosciences.
[47] L Naldini,et al. Highly efficient and sustained gene transfer in adult neurons with a lentivirus vector , 1997, Journal of virology.
[48] M. Chesselet,et al. Decrease in Striatal Enkephalin mRNA in Mouse Models of Huntington’s Disease , 2000, Experimental Neurology.
[49] M. Hurlbert,et al. Mice transgenic for an expanded CAG repeat in the Huntington's disease gene develop diabetes. , 1999, Diabetes.
[50] G. Pearlson,et al. Rate of caudate atrophy in presymptomatic and symptomatic stages of Huntington's disease , 2000, Movement disorders : official journal of the Movement Disorder Society.
[51] J. Mandel,et al. A cellular model that recapitulates major pathogenic steps of Huntington's disease. , 1998, Human molecular genetics.
[52] R. Albin,et al. Neurological abnormalities in a knock-in mouse model of Huntington's disease. , 2001, Human molecular genetics.
[53] Manish S. Shah,et al. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes , 1993, Cell.
[54] A. Hottinger,et al. Complete and Long-Term Rescue of Lesioned Adult Motoneurons by Lentiviral-Mediated Expression of Glial Cell Line-Derived Neurotrophic Factor in the Facial Nucleus , 2000, The Journal of Neuroscience.
[55] J. Brandt,et al. Reduced basal ganglia volume associated with the gene for Huntington's disease in asymptomatic at‐risk persons , 1994, Neurology.
[56] A Dürr,et al. Spinocerebellar ataxia type 7 (SCA7): a neurodegenerative disorder with neuronal intranuclear inclusions. , 1998, Human molecular genetics.
[57] S. Hersch,et al. Huntington aggregates may not predict neuronal death in Huntington's disease. , 1999, Annals of neurology.
[58] C A Ross,et al. Decreased expression of striatal signaling genes in a mouse model of Huntington's disease. , 2000, Human molecular genetics.
[59] P. Greengard,et al. Beyond the Dopamine Receptor: Review the DARPP-32/Protein Phosphatase-1 Cascade , 1999 .
[60] L. Schmued,et al. Fluoro-Jade B: a high affinity fluorescent marker for the localization of neuronal degeneration , 2000, Brain Research.
[61] Jacqueline K. White,et al. Length-dependent gametic CAG repeat instability in the Huntington's disease knock-in mouse. , 1999, Human molecular genetics.
[62] R. Mulligan,et al. A stable human-derived packaging cell line for production of high titer retrovirus/vesicular stomatitis virus G pseudotypes. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[63] J. Bloch,et al. Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease. , 2000, Science.
[64] William Slikker,et al. Fluoro-Jade: a novel fluorochrome for the sensitive and reliable histochemical localization of neuronal degeneration , 1997, Brain Research.
[65] C. Blakemore,et al. N‐Acetylaspartate and DARPP‐32 levels decrease in the corpus striatum of Huntington's disease mice , 2000, Neuroreport.
[66] D. Price,et al. Transglutaminase aggregates huntingtin into nonamyloidogenic polymers, and its enzymatic activity increases in Huntington's disease brain nuclei. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[67] H. Paulson. Toward an Understanding of Polyglutamine Neurodegeneration , 2000, Brain pathology.
[68] H. Johnston,et al. A Huntington's disease CAG expansion at the murine Hdh locus is unstable and associated with behavioural abnormalities in mice. , 1999, Human molecular genetics.
[69] O. Suchowersky,et al. Relationship between trinucleotide repeats and neuropathological changes in Huntington's disease. , 1996, Annals of neurology.
[70] F. Gage,et al. Lentiviral vectors: regulated gene expression. , 2000, Molecular therapy : the journal of the American Society of Gene Therapy.
[71] J. Mazziotta,et al. Reduced cerebral glucose metabolism in asymptomatic subjects at risk for Huntington's disease. , 1987, The New England journal of medicine.