PAR-1 Kinase Plays an Initiator Role in a Temporally Ordered Phosphorylation Process that Confers Tau Toxicity in Drosophila
暂无分享,去创建一个
[1] E. Mandelkow,et al. MARKK, a Ste20‐like kinase, activates the polarity‐inducing kinase MARK/PAR‐1 , 2003, The EMBO journal.
[2] M. Mattson,et al. Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles Intracellular Aβ and Synaptic Dysfunction , 2003, Neuron.
[3] Kazuyuki Takata,et al. Cdk5 Is a Key Factor in Tau Aggregation and Tangle Formation In Vivo , 2003, Neuron.
[4] Isao Nishimura,et al. Parkin Suppresses Dopaminergic Neuron-Selective Neurotoxicity Induced by Pael-R in Drosophila , 2003, Neuron.
[5] Y. Jan,et al. Hippocampal Neuronal Polarity Specified by Spatially Localized mPar3/mPar6 and PI 3-Kinase Activity , 2003, Cell.
[6] G. Seydoux,et al. Anterior-Posterior Polarity in C. elegans and Drosophila--PARallels and Differences , 2002, Science.
[7] E. Mandelkow,et al. Protein kinase MARK/PAR-1 is required for neurite outgrowth and establishment of neuronal polarity. , 2002, Molecular biology of the cell.
[8] D. Selkoe. Alzheimer's Disease Is a Synaptic Failure , 2002, Science.
[9] I. Grundke‐Iqbal,et al. Involvement of aberrant glycosylation in phosphorylation of tau by cdk5 and GSK‐3β , 2002, FEBS letters.
[10] D. Selkoe,et al. The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics , 2002, Science.
[11] D. Geschwind,et al. Human Wild-Type Tau Interacts with wingless Pathway Components and Produces Neurofibrillary Pathology in Drosophila , 2002, Neuron.
[12] A. Ephrussi,et al. Par-1 regulates stability of the posterior determinant Oskar by phosphorylation , 2002, Nature Cell Biology.
[13] M. Fortini,et al. Gene expression pattern Identification and characterization of the Drosophila tau homolog , 2001 .
[14] R. Nitsch,et al. Formation of Neurofibrillary Tangles in P301L Tau Transgenic Mice Induced by Aβ42 Fibrils , 2001, Science.
[15] J. Hardy,et al. Enhanced Neurofibrillary Degeneration in Transgenic Mice Expressing Mutant Tau and APP , 2001, Science.
[16] Yuh Nung Jan,et al. PAR-1 is a Dishevelled-associated kinase and a positive regulator of Wnt signalling , 2001, Nature Cell Biology.
[17] Joshua M. Shulman,et al. Tauopathy in Drosophila: Neurodegeneration Without Neurofibrillary Tangles , 2001, Science.
[18] Y. Jan,et al. Drosophila par-1 is required for oocyte differentiation and microtubule organization , 2001, Current Biology.
[19] René Hen,et al. Decreased nuclear β‐catenin, tau hyperphosphorylation and neurodegeneration in GSK‐3β conditional transgenic mice , 2001 .
[20] M. Mercken,et al. Glycogen Synthase Kinase-3β Phosphorylates Protein Tau and Rescues the Axonopathy in the Central Nervous System of Human Four-repeat Tau Transgenic Mice* , 2000, The Journal of Biological Chemistry.
[21] P. Davies. A Very Incomplete Comprehensive Theory of Alzheimer's Disease , 2000, Annals of the New York Academy of Sciences.
[22] Wen-Lang Lin,et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein , 2000, Nature Genetics.
[23] Pavel Tomancak,et al. A Drosophila melanogaster homologue of Caenorhabditis elegans par-1 acts at an early step in embryonic-axis formation , 2000, Nature Cell Biology.
[24] M. Gall,et al. The cyclin-dependent kinase Cdk5 controls multiple aspects of axon patterning in vivo , 2000, Current Biology.
[25] Richard Benton,et al. The Drosophila Homolog of C. elegans PAR-1 Organizes the Oocyte Cytoskeleton and Directs oskar mRNA Localization to the Posterior Pole , 2000, Cell.
[26] G. Johnson,et al. Microtubule/MAP‐Affinity Regulating Kinase (MARK) Is Activated by Phenylarsine Oxide In Situ and Phosphorylates Tau Within Its Microtubule‐Binding Domain , 2000, Journal of neurochemistry.
[27] B. Dickson,et al. Analysis of Drosophila photoreceptor axon guidance in eye-specific mosaics. , 2000, Development.
[28] L. Tsai,et al. Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration , 1999, Nature.
[29] E. Mandelkow,et al. Alzheimer's disease: The tangled tale of tau , 1999, Nature.
[30] Bin Zhang,et al. Age-Dependent Emergence and Progression of a Tauopathy in Transgenic Mice Overexpressing the Shortest Human Tau Isoform , 1999, Neuron.
[31] Liqun Luo,et al. Mosaic Analysis with a Repressible Cell Marker for Studies of Gene Function in Neuronal Morphogenesis , 1999, Neuron.
[32] E. Mandelkow,et al. Tau in Alzheimer's disease. , 1998, Trends in cell biology.
[33] A Klug,et al. Mutation in the tau gene in familial multiple system tauopathy with presenile dementia. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[34] Ronald C. Petersen,et al. Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17 , 1998, Nature.
[35] G. Schellenberg,et al. Tau is a candidate gene for chromosome 17 frontotemporal dementia , 1998, Annals of neurology.
[36] K. Imahori,et al. Characterization of tau phosphorylation in glycogen synthase kinase-3beta and cyclin dependent kinase-5 activator (p23) transfected cells. , 1998, Biochimica et biophysica acta.
[37] E. Mandelkow,et al. Sequential phosphorylation of Tau by glycogen synthase kinase-3beta and protein kinase A at Thr212 and Ser214 generates the Alzheimer-specific epitope of antibody AT100 and requires a paired-helical-filament-like conformation. , 1998, European journal of biochemistry.
[38] M. Drab,et al. Mammalian homologues of C. elegans PAR-1 are asymmetrically localized in epithelial cells and may influence their polarity , 1997, Current Biology.
[39] N L Foster,et al. Frontotemporal dementia and parkinsonism linked to chromosome 17: A consensus conference , 1997, Annals of neurology.
[40] G. Drewes,et al. MARK, a Novel Family of Protein Kinases That Phosphorylate Microtubule-Associated Proteins and Trigger Microtubule Disruption , 1997, Cell.
[41] D. Dickson,et al. Neurodegenerative disorders with extensive tau pathology: A comparative study and review , 1996, Annals of neurology.
[42] M. Goedert,et al. Tau protein is phosphorylated by cyclic AMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase II within its microtubule-binding domains at Ser-262 and Ser-356. , 1996, The Biochemical journal.
[43] A. Mccarthy. Development , 1996, Current Opinion in Neurobiology.
[44] J. Ávila,et al. Glycogen synthase kinase 3 phosphorylates recombinant human tau protein at serine‐262 in the presence of heparin (or tubulin) , 1995, FEBS letters.
[45] J. Trojanowski,et al. Detection of Phosphorylated Ser262 in Fetal Tau, Adult Tau, and Paired Helical Filament Tau (*) , 1995, The Journal of Biological Chemistry.
[46] P. Cohen,et al. Molecular dissection of the paired helical filament , 1995, Neurobiology of Aging.
[47] K. Kemphues,et al. par-1, a gene required for establishing polarity in C. elegans embryos, encodes a putative Ser/Thr kinase that is asymmetrically distributed , 1995, Cell.
[48] E. Mandelkow,et al. Microtubule-associated Protein/Microtubule Affinity-regulating Kinase (p110mark) , 1995, The Journal of Biological Chemistry.
[49] Simon Lovestone,et al. Alzheimer's disease-like phosphorylation of the microtubule-associated protein tau by glycogen synthase kinase-3 in transfected mammalian cells , 1994, Current Biology.
[50] N. Perrimon,et al. Targeted gene expression as a means of altering cell fates and generating dominant phenotypes. , 1993, Development.
[51] H. Braak,et al. Neuropathological stageing of Alzheimer-related changes , 2004, Acta Neuropathologica.
[52] M. Goedert. Neurofibrillary pathology of Alzheimer's disease and other tauopathies. , 1998, Progress in brain research.