The beta-amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism. - Wikidata - awgldk - TriplyDB

The beta-amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism.

The beta-amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism.

http://www.wikidata.org/entity/Q46902000

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Recent developments of protein kinase inhibitors as potential AD therapeutics Mechanisms of synapse and dendrite maintenance and their disruption in psychiatric and neurodegenerative disorders Regulation of the Postsynaptic Compartment of Excitatory Synapses by the Actin Cytoskeleton in Health and Its Disruption in Disease Protein prenylation and synaptic plasticity: implications for Alzheimer's disease The Beta-amyloid protein of Alzheimer's disease: communication breakdown by modifying the neuronal cytoskeleton Rho family GTPases: key players in neuronal development, neuronal survival, and neurodegeneration Crystal and solution structure, stability and post-translational modifications of collapsin response mediator protein 2 PAK in Alzheimer disease, Huntington disease and X-linked mental retardation Leukocyte common antigen-related phosphatase is a functional receptor for chondroitin sulfate proteoglycan axon growth inhibitors RhoGTPase Regulators Orchestrate Distinct Stages of Synaptic Development.Vertebrate paralogous CRMPs in nervous system: evolutionary, structural, and functional interplay.Automated imaging system for fast quantitation of neurons, cell morphology and neurite morphometry in vivo and in vitro.Quantitative proteomics analysis of inborn errors of cholesterol synthesis: identification of altered metabolic pathways in DHCR7 and SC5D deficiency Cellular levels of Grb2 and cytoskeleton stability are correlated in a neurodegenerative scenario.A novel unbiased proteomic approach to detect the reactivity of cerebrospinal fluid in neurological diseases The metabolic enhancer piracetam ameliorates the impairment of mitochondrial function and neurite outgrowth induced by beta-amyloid peptide Isoprenoids, small GTPases and Alzheimer's disease.Interleukin-18 alters protein expressions of neurodegenerative diseases-linked proteins in human SH-SY5Y neuron-like cells Elucidating the role of DEPTOR in Alzheimer's disease.Axonal degeneration in multiple sclerosis: can we predict and prevent permanent disability?Quantitative proteomics analysis of phosphorylated proteins in the hippocampus of Alzheimer's disease subjects.Rac1b increases with progressive tau pathology within cholinergic nucleus basalis neurons in Alzheimer's disease.Collapsin response mediator protein-2 phosphorylation promotes the reversible retraction of oligodendrocyte processes in response to non-lethal oxidative stress.The dynamics of Rho GTPase signaling and implications for targeting cancer and the tumor microenvironment.The protection of acetylcholinesterase inhibitor on β-amyloid-induced the injury of neurite outgrowth via regulating axon guidance related genes expression in neuronal cells.Propagation of Neuronal Damage to Embryonic Grafts Transplanted in the Hippocampus of Murine Models of Alzheimer's Disease.Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation.The therapeutic effects of Rho-ROCK inhibitors on CNS disorders.Collapsin Response Mediator Protein-2 (CRMP2) is a Plausible Etiological Factor and Potential Therapeutic Target in Alzheimer's Disease: Comparison and Contrast with Microtubule-Associated Protein Tau STX, a Novel Membrane Estrogen Receptor Ligand, Protects Against Amyloid-β Toxicity.RhoA Signaling and Synaptic Damage Occur Within Hours in a Live Pig Model of CNS Injury, Retinal Detachment.Reactive oxygen species induce neurite degeneration before induction of cell death.Semaphorin function in neural plasticity and disease.Annexin A1 restores Aβ1-42 -induced blood-brain barrier disruption through the inhibition of RhoA-ROCK signaling pathway.NO orchestrates the loss of synaptic boutons from adult "sick" motoneurons: modeling a molecular mechanism.Neuroproteomics approach and neurosystems biology analysis: ROCK inhibitors as promising therapeutic targets in neurodegeneration and neurotrauma.Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.Reversing synapse loss in Alzheimer's disease: Rho-guanosine triphosphatases and insights from other brain disorders.Postnatal alteration of collapsin response mediator protein 4 mRNA expression in the mouse brain.Function of Nogo-A/Nogo-A receptor in Alzheimer's disease.

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The beta-amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism.

http://www.wikidata.org/entity/Q46902000

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年學術文章

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name

The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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type

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The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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The beta-amyloid protein of Al ...... lation by a Rho-GTP mechanism.

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Danuta Maksel

http://www.w3.org/2001/XMLSchema#string

David H Small

http://www.w3.org/2001/XMLSchema#string

Irene Hatzinisiriou

http://www.w3.org/2001/XMLSchema#string

Megan L Kerr

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Qiao-Xin Li

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Sharon E Unabia

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Steven Petratos

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Xu Hou

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P2860

Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE

Purification and cloning of amyloid precursor protein beta-secretase from human brain

A Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides

A novel gene family defined by human dihydropyrimidinase and three related proteins with differential tissue distribution

Distinct priming kinases contribute to differential regulation of collapsin response mediator proteins by glycogen synthase kinase-3 in vivo

Structural bases for CRMP function in plexin-dependent semaphorin3A signaling

CRMP-2 regulates polarized Numb-mediated endocytosis for axon growth.

LINGO-1 is a component of the Nogo-66 receptor/p75 signaling complex.

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90-108

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scholarly article

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10.1093/BRAIN/AWM260

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Pt 1

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131

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Marie-Isabel Aguilar

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2007-11-13T00:00:00Z

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18000012

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phosphorylation