Tau reduction prevents A-induced axonal transport deficits by blocking activation of GSK 3
暂无分享,去创建一个
Keith A. Vossel | K. Vossel | L. Mucke | T. Miyamoto | Kaitlyn Ho | Daniel H. Kim | Lennart Mucke | Daniel H. Kim | Gui-Qiu Yu | Jordan C. Xu | Vira Fomenko | Takashi Miyamoto | Elsa Suberbielle | Joseph A. Knox | Kaitlyn Ho | Elsa Suberbielle | Gui-qiu Yu | V. Fomenko
[1] L. Mucke,et al. Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease , 2008, Nature Neuroscience.
[2] P. Greengard,et al. Regulation of NMDA receptor trafficking by amyloid-β , 2005, Nature Neuroscience.
[3] M. Rasenick,et al. Tau associates with actin in differentiating PC12 cells , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[4] E. Mandelkow,et al. Amyloid‐β oligomers induce synaptic damage via Tau‐dependent microtubule severing by TTLL6 and spastin , 2013, The EMBO journal.
[5] M. Zvelebil,et al. Phosphorylation Regulates Tau Interactions with Src Homology 3 Domains of Phosphatidylinositol 3-Kinase, Phospholipase Cγ1, Grb2, and Src Family Kinases* , 2008, Journal of Biological Chemistry.
[6] M. Feany,et al. Tau Promotes Neurodegeneration via DRP1 Mislocalization In Vivo , 2012, Neuron.
[7] H. Paudel,et al. Glycogen Synthase Kinase-3β Is Complexed with Tau Protein in Brain Microtubules* , 2002, The Journal of Biological Chemistry.
[8] J. Macdonald,et al. Regulation of NMDA receptors by the tyrosine kinase Fyn , 2012, The FEBS journal.
[9] Adriana B Ferreira,et al. β-Amyloid-induced Dynamin 1 Degradation Is Mediated by N-Methyl-D-Aspartate Receptors in Hippocampal Neurons* , 2006, Journal of Biological Chemistry.
[10] M. Kneussel,et al. Neuronal depolarization modifies motor protein mobility , 2009, Neuroscience.
[11] A. Erisir,et al. Tau-dependent microtubule disassembly initiated by prefibrillar β-amyloid , 2006, The Journal of cell biology.
[12] M. Vitek,et al. Tau is essential to β-amyloid-induced neurotoxicity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[13] F. van Leuven,et al. Amyloid activates GSK-3beta to aggravate neuronal tauopathy in bigenic mice. , 2008, The American journal of pathology.
[14] Jürgen Götz,et al. Parkinsonism and impaired axonal transport in a mouse model of frontotemporal dementia , 2008, Proceedings of the National Academy of Sciences.
[15] A. Reith,et al. Selective small-molecule inhibitors of glycogen synthase kinase-3 activity protect primary neurones from death. , 2001 .
[16] G. Collingridge,et al. LTP Inhibits LTD in the Hippocampus via Regulation of GSK3β , 2007, Neuron.
[17] Elyssa B. Margolis,et al. Loss of Mitochondrial Fission Depletes Axonal Mitochondria in Midbrain Dopamine Neurons , 2014, The Journal of Neuroscience.
[18] Xiongwei Zhu,et al. Amyloid-β-Derived Diffusible Ligands Cause Impaired Axonal Transport of Mitochondria in Neurons , 2010, Neurodegenerative Diseases.
[19] J W Yates,et al. Selective small molecule inhibitors of glycogen synthase kinase-3 modulate glycogen metabolism and gene transcription. , 2000, Chemistry & biology.
[20] Y. Toyoshima,et al. Regulation of Mitochondrial Transport and Inter-Microtubule Spacing by Tau Phosphorylation at the Sites Hyperphosphorylated in Alzheimer's Disease , 2012, The Journal of Neuroscience.
[21] L. Farrer,et al. Identification of Alzheimer disease-associated variants in genes that regulate retromer function , 2012, Neurobiology of Aging.
[22] P. Cohen,et al. Inactivation of glycogen synthase kinase-3 beta by phosphorylation: new kinase connections in insulin and growth-factor signalling. , 1993, The Biochemical journal.
[23] E. Fernandes,et al. MDMA impairs mitochondrial neuronal trafficking in a Tau- and Mitofusin2/Drp1-dependent manner , 2014, Archives of Toxicology.
[24] Gloria Lee,et al. Tau Potentiates Nerve Growth Factor-induced Mitogen-activated Protein Kinase Signaling and Neurite Initiation without a Requirement for Microtubule Binding* , 2010, The Journal of Biological Chemistry.
[25] S. Ferreira,et al. Amyloid-β oligomers induce tau-independent disruption of BDNF axonal transport via calcineurin activation in cultured hippocampal neurons , 2013, Molecular biology of the cell.
[26] G. Bloom,et al. Amyloid-&bgr; signals through tau to drive ectopic neuronal cell cycle re-entry in Alzheimer's disease , 2013, Journal of Cell Science.
[27] R. Dolmetsch,et al. Calcium Imaging of Cortical Neurons using Fura-2 AM , 2009, Journal of visualized experiments : JoVE.
[28] W. Klein,et al. Deleterious Effects of Amyloid β Oligomers Acting as an Extracellular Scaffold for mGluR5 , 2010, Neuron.
[29] E. Mandelkow,et al. Aβ Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines , 2010, The Journal of Neuroscience.
[30] S. Ferreira,et al. Amyloid-β Peptide Oligomers Disrupt Axonal Transport through an NMDA Receptor-Dependent Mechanism That Is Mediated by Glycogen Synthase Kinase 3β in Primary Cultured Hippocampal Neurons , 2010, The Journal of Neuroscience.
[31] W. Klein,et al. Aβ Oligomers Induce Neuronal Oxidative Stress through an N-Methyl-D-aspartate Receptor-dependent Mechanism That Is Blocked by the Alzheimer Drug Memantine* , 2007, Journal of Biological Chemistry.
[32] Jürgen Götz,et al. Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models , 2010, Cell.
[33] Hans-Ulrich Demuth,et al. Prion-Like Behavior and Tau-dependent Cytotoxicity of Pyroglutamylated β-Amyloid , 2012, Nature.
[34] T. Sawada,et al. Involvement of microtubule integrity in memory impairment caused by colchicine , 2002, Pharmacology Biochemistry and Behavior.
[35] Julie Harris,et al. Reversing EphB2 depletion rescues cognitive functions in Alzheimer model , 2011, Nature.
[36] D. Holtzman,et al. Antisense Reduction of Tau in Adult Mice Protects against Seizures , 2013, The Journal of Neuroscience.
[37] M. McNiven,et al. The Mitochondrial Protein hFis1 Regulates Mitochondrial Fission in Mammalian Cells through an Interaction with the Dynamin-Like Protein DLP1 , 2003, Molecular and Cellular Biology.
[38] H. Paudel,et al. 14-3-3 Connects Glycogen Synthase Kinase-3β to Tau within a Brain Microtubule-associated Tau Phosphorylation Complex* , 2003, The Journal of Biological Chemistry.
[39] V. Laporte,et al. Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice. , 2012, The American journal of pathology.
[40] Meaghan Morris,et al. The Many Faces of Tau , 2011, Neuron.
[41] Kai Zhang,et al. Tau Reduction Prevents Aβ-Induced Defects in Axonal Transport , 2010, Science.
[42] Kang Hu,et al. High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation , 2000, The Journal of Neuroscience.
[43] Xiongwei Zhu,et al. Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins , 2008, Proceedings of the National Academy of Sciences.
[44] R. Lasek,et al. Axonal tubulin and axonal microtubules: biochemical evidence for cold stability , 1984, Journal of Cell Biology.
[45] S. Younkin,et al. Tau Loss Attenuates Neuronal Network Hyperexcitability in Mouse and Drosophila Genetic Models of Epilepsy , 2013, The Journal of Neuroscience.
[46] H. Feldman,et al. Pharmacodynamics of Selective Inhibition of γ-Secretase by Avagacestat , 2013, The Journal of Pharmacology and Experimental Therapeutics.
[47] Julie R. Leitz,et al. Tau Protein Is Required for Amyloid β-Induced Impairment of Hippocampal Long-Term Potentiation , 2011, The Journal of Neuroscience.
[48] E. Mandelkow,et al. The 'jaws' model of tau-microtubule interaction examined in CHO cells. , 1997, Journal of cell science.
[49] A. Sun,et al. Deletion of tau attenuates heat shock‐induced injury in cultured cortical neurons , 2010, Journal of neuroscience research.
[50] Nancy Ratner,et al. Glycogen synthase kinase 3 phosphorylates kinesin light chains and negatively regulates kinesin‐based motility , 2002, The EMBO journal.
[51] E. Aronica,et al. Induction of Dickkopf-1, a Negative Modulator of the Wnt Pathway, Is Associated with Neuronal Degeneration in Alzheimer's Brain , 2004, The Journal of Neuroscience.
[52] G. Perry,et al. Identification and transport of full-length amyloid precursor proteins in rat peripheral nervous system , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[53] U. Landegren,et al. Direct observation of individual endogenous protein complexes in situ by proximity ligation , 2006, Nature Methods.
[54] Subhojit Roy,et al. Early and Selective Impairments in Axonal Transport Kinetics of Synaptic Cargoes Induced by Soluble Amyloid β‐Protein Oligomers , 2012, Traffic.
[55] Anatol C. Kreitzer,et al. Physiological Brain Activity Causes DNA Double Strand Breaks in Neurons — Exacerbation by Amyloid-β , 2013, Nature Neuroscience.
[56] Aidong Yuan,et al. Axonal Transport Rates In Vivo Are Unaffected by Tau Deletion or Overexpression in Mice , 2008, The Journal of Neuroscience.
[57] R. Malinow,et al. Metabotropic NMDA receptor function is required for β-amyloid–induced synaptic depression , 2013, Proceedings of the National Academy of Sciences.
[58] H. Band,et al. Tau interacts with src-family non-receptor tyrosine kinases. , 1998, Journal of cell science.
[59] T. Kawakami,et al. Glutamate and Amyloid β-Protein Rapidly Inhibit Fast Axonal Transport in Cultured Rat Hippocampal Neurons by Different Mechanisms , 2003, The Journal of Neuroscience.
[60] L. Mucke,et al. Collagen VI protects neurons against Aβ toxicity , 2009, Nature Neuroscience.
[61] George Perry,et al. Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer's Disease , 2009, The Journal of Neuroscience.
[62] A. Godzik,et al. S-Nitrosylation of Drp1 Mediates β-Amyloid-Related Mitochondrial Fission and Neuronal Injury , 2009, Science.
[63] G. Schellenberg,et al. Tau isoform regulation is region‐ and cell‐specific in mouse brain , 2008, The Journal of comparative neurology.
[64] Arthur Konnerth,et al. Clusters of Hyperactive Neurons Near Amyloid Plaques in a Mouse Model of Alzheimer's Disease , 2008, Science.
[65] M. Vitek,et al. Inhibition of neuronal maturation in primary hippocampal neurons from tau deficient mice. , 2001, Journal of cell science.
[66] S. Lawler,et al. Physiological transgene regulation and functional complementation of a neurological disease gene deficiency in neurons. , 2009, Molecular Therapy.
[67] David Baltimore,et al. Germline Transmission and Tissue-Specific Expression of Transgenes Delivered by Lentiviral Vectors , 2002, Science.
[68] S. Lipton,et al. Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss , 2013, Proceedings of the National Academy of Sciences.
[69] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[70] Priyanka Tiwari,et al. Acute Impairment of Mitochondrial Trafficking by β-Amyloid Peptides in Hippocampal Neurons , 2006, Journal of Neuroscience.
[71] K. Imahori,et al. Exposure of rat hippocampal neurons to amyloid β peptide (25–35) induces the inactivation of phosphatidyl inositol-3 kinase and the activation of tau protein kinase I/glycogen synthase kinase-3β , 1996, Neuroscience Letters.
[72] Shaomin Li,et al. Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake , 2009, Neuron.
[73] Meaghan Morris,et al. Age-appropriate cognition and subtle dopamine-independent motor deficits in aged Tau knockout mice , 2013, Neurobiology of Aging.
[74] E. Rugarli,et al. Loss of the m‐AAA protease subunit AFG3L2 causes mitochondrial transport defects and tau hyperphosphorylation , 2014, The EMBO journal.
[75] Xinnan Wang,et al. The Mechanism of Ca2+-Dependent Regulation of Kinesin-Mediated Mitochondrial Motility , 2009, Cell.
[76] Bin Zhang,et al. Retarded Axonal Transport of R406W Mutant Tau in Transgenic Mice with a Neurodegenerative Tauopathy , 2004, The Journal of Neuroscience.
[77] A. Kozikowski,et al. The amino terminus of tau inhibits kinesin‐dependent axonal transport: Implications for filament toxicity , 2009, Journal of neuroscience research.
[78] A. Andreadis,et al. Phosphorylation in the amino terminus of tau prevents inhibition of anterograde axonal transport , 2012, Neurobiology of Aging.
[79] L. Mucke,et al. Amyloid-β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease , 2011, The Journal of Neuroscience.
[80] H. Beck,et al. Stable Mossy Fiber Long-Term Potentiation Requires Calcium Influx at the Granule Cell Soma, Protein Synthesis, and Microtubule-Dependent Axonal Transport , 2010, The Journal of Neuroscience.
[81] N. Chabot,et al. Transglutaminase and Polyamination of Tubulin: Posttranslational Modification for Stabilizing Axonal Microtubules , 2013, Neuron.
[82] S. Pulst,et al. Loss of Miro1-directed mitochondrial movement results in a novel murine model for neuron disease , 2014, Proceedings of the National Academy of Sciences.
[83] D. Selkoe,et al. Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration , 2011, Proceedings of the National Academy of Sciences.
[84] R. Motter,et al. Amyloid precursor protein processing and Aβ42 deposition in a transgenic mouse model of Alzheimer disease , 1997 .
[85] G. Collingridge,et al. Microtubule-associated protein tau is essential for long-term depression in the hippocampus , 2014, Philosophical Transactions of the Royal Society B: Biological Sciences.
[86] Bradley T. Hyman,et al. Specific tau phosphorylation sites correlate with severity of neuronal cytopathology in Alzheimer's disease , 2014, Acta Neuropathologica.
[87] L. Mucke,et al. Tau Reduction Prevents Disease in a Mouse Model of Dravet Syndrome , 2014, Annals of neurology.
[88] P. Reddy,et al. Amyloid beta impairs mitochondrial anterograde transport and degenerates synapses in Alzheimer's disease neurons. , 2011, Biochimica et biophysica acta.
[89] F. Herrmann. 34 Cognitive reserve and survival , 2012, Neurobiology of Aging.
[90] G. V. Van Hoesen,et al. Phosphorylation of Tau by Fyn: Implications for Alzheimer's Disease , 2004, The Journal of Neuroscience.
[91] Sandra A G Visser,et al. Decreased axonal transport rates in the Tg2576 APP transgenic mouse: improvement with the gamma‐secretase inhibitor MRK‐560 as detected by manganese‐enhanced MRI , 2012, The European journal of neuroscience.
[92] M. Frotscher,et al. Tau's role in the developing brain: implications for intellectual disability. , 2012, Human molecular genetics.
[93] A. Andreadis,et al. Pathogenic Forms of Tau Inhibit Kinesin-Dependent Axonal Transport through a Mechanism Involving Activation of Axonal Phosphotransferases , 2011, The Journal of Neuroscience.
[94] G. Collingridge,et al. Aβ1–42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β , 2011, Nature Neuroscience.
[95] R. He,et al. The proline-rich domain of tau plays a role in interactions with actin , 2009, BMC Cell Biology.