Transgenic mouse models and human neurodegenerative disorders.
暂无分享,去创建一个
T. Siddique | H. Deng | H X Deng | T Siddique
[1] T. Noda,et al. Loss of cerebellar Purkinje cells in aged mice homozygous for a disrupted PrP gene , 1996, Nature.
[2] I. Mcconnell,et al. PrP gene dosage determines the timing but not the final intensity or distribution of lesions in scrapie pathology. , 1994, Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration.
[3] D C Wight,et al. Transgenic mice: a decade of progress in technology and research. , 1994, Mutation research.
[4] Hans Clevers,et al. Destabilization of β-catenin by mutations in presenilin-1 potentiates neuronal apoptosis , 1998, Nature.
[5] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[6] M. Beal,et al. Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury , 1996, Nature Genetics.
[7] D. Borchelt,et al. An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria , 1995, Neuron.
[8] M. Dubois‐Dauphin,et al. Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. , 1997, Science.
[9] J. Morrison,et al. Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[10] L. Mucke,et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.
[11] A. Plück. Conditional mutagenesis in mice: the Cre/loxP recombination system. , 1996, International journal of experimental pathology.
[12] H. Zoghbi,et al. Expanding Our Understanding of Polyglutamine Diseases through Mouse Models , 1999, Neuron.
[13] H. Zoghbi,et al. Mice Lacking Ataxin-1 Display Learning Deficits and Decreased Hippocampal Paired-Pulse Facilitation , 1998, The Journal of Neuroscience.
[14] A. Aguzzi,et al. Mice devoid of PrP are resistant to scrapie , 1993, Cell.
[15] Harry T Orr,et al. Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice , 1999, Neuron.
[16] Junying Yuan,et al. Inhibition of ICE slows ALS in mice , 1997, Nature.
[17] S. Prusiner,et al. Transmission of Creutzfeldt-Jakob disease from humans to transgenic mice expressing chimeric human-mouse prion protein. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[18] P. Wong,et al. Pathogenesis of two axonopathies does not require axonal neurofilaments , 1998, Nature.
[19] S. Tonegawa,et al. Skeletal and CNS Defects in Presenilin-1-Deficient Mice , 1997, Cell.
[20] S. Prusiner,et al. Serial transmission in rodents of neurodegeneration from transgenic mice expressing mutant prion protein. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[21] Q. Zhu,et al. Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[22] J. Hardy,et al. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes , 1998, Nature Medicine.
[23] M. Gurney,et al. Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. , 1994, Science.
[24] D. Schiffer,et al. Lack of apoptosis in mice with ALS , 1999, Nature Medicine.
[25] Harry T Orr,et al. Ataxin-1 Nuclear Localization and Aggregation Role in Polyglutamine-Induced Disease in SCA1 Transgenic Mice , 1998, Cell.
[26] L. Bruijn,et al. Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. , 1998, Science.
[27] 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.
[28] J. Hardy,et al. Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.
[29] 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.
[30] D. Borchelt,et al. Caspase-1 is activated in neural cells and tissue with amyotrophic lateral sclerosis-associated mutations in copper-zinc superoxide dismutase. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[31] Christian von Mering,et al. Expression of Amino-Terminally Truncated PrP in the Mouse Leading to Ataxia and Specific Cerebellar Lesions , 1998, Cell.
[32] Weiming Xia,et al. Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice , 1997, Nature Medicine.
[33] Q. Zhu,et al. Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[34] B. Hogan,et al. Manipulating the mouse embryo: A laboratory manual , 1986 .
[35] Harry T Orr,et al. SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat , 1995, Cell.