Therapeutic molecules and endogenous ligands regulate the interaction between brain cellular prion protein (PrPC) and metabotropic glutamate receptor 5 (mGluR5).
about
A specific nanobody prevents amyloidogenesis of D76N β2-microglobulin in vitro and modifies its tissue distribution in vivo.Fyn inhibition rescues established memory and synapse loss in Alzheimer mice.Dextran sulfate sodium inhibits amyloid-β oligomer binding to cellular prion protein.Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models.Metabotropic glutamate receptor 5 couples cellular prion protein to intracellular signalling in Alzheimer's diseaseThe Biological Function of the Prion Protein: A Cell Surface Scaffold of Signaling ModulesPhysiological Functions of the Cellular Prion Protein.Glutamate receptors function as scaffolds for the regulation of β-amyloid and cellular prion protein signaling complexes.Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer's Mouse Phenotypes.Group I Metabotropic Glutamate Receptor Interacting Proteins: Fine-Tuning Receptor Functions in Health and Disease.Regulation of Amyloid β Oligomer Binding to Neurons and Neurotoxicity by the Prion Protein-mGluR5 Complex.Oligomers of Amyloid β Prevent Physiological Activation of the Cellular Prion Protein-Metabotropic Glutamate Receptor 5 Complex by Glutamate in Alzheimer Disease.Ca(2+)/calmodulin-dependent protein kinase II interacts with group I metabotropic glutamate and facilitates receptor endocytosis and ERK1/2 signaling: role of β-amyloid.Cellular prion protein targets amyloid-β fibril ends via its C-terminal domain to prevent elongation.Inhibition of group-I metabotropic glutamate receptors protects against prion toxicity.Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease.Correction of Huntington's Disease Phenotype by Genistein-Induced Autophagy in the Cellular Model.Liquid and Hydrogel Phases of PrP Linked to Conformation Shifts and Triggered by Alzheimer's Amyloid-β Oligomers
P2860
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P2860
Therapeutic molecules and endogenous ligands regulate the interaction between brain cellular prion protein (PrPC) and metabotropic glutamate receptor 5 (mGluR5).
description
2014 nî lūn-bûn
@nan
2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2014 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
name
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@ast
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@en
Therapeutic molecules and endo ...... n brain cellular prion protein
@nl
type
label
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@ast
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@en
Therapeutic molecules and endo ...... n brain cellular prion protein
@nl
prefLabel
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@ast
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@en
Therapeutic molecules and endo ...... n brain cellular prion protein
@nl
P2860
P356
P1476
Therapeutic molecules and endo ...... glutamate receptor 5 (mGluR5).
@en
P2093
Laura T Haas
P2860
P304
28460-28477
P356
10.1074/JBC.M114.584342
P407
P577
2014-08-22T00:00:00Z