Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathways (Q28575781)

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English	Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathways	scientific journal article

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31 January 2017

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1 February 2020

Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathways (English)

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31 January 2017

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1 February 2020

Francesco Roselli

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Osborne F.X. Almeida

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1 February 2020

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Peter Hutzler

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1 February 2020

Yvonne Wegerich

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23 June 2009

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1 February 2020

4

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23 June 2009

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The postsynaptic density proteins Homer and Shank form a polymeric network structure

1 reference

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Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1.

1 reference

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

1 reference

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An architectural framework that may lie at the core of the postsynaptic density

1 reference

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Surface clustering of metabotropic glutamate receptor 1 induced by long Homer proteins

1 reference

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1 reference

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1 reference

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Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway

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1 reference

https://pubmed.ncbi.nlm.nih.gov/19547699

12 December 2020

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Differential control of postsynaptic density scaffolds via actin-dependent and -independent mechanisms

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https://pubmed.ncbi.nlm.nih.gov/19547699

12 December 2020

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10.1371/JOURNAL.PONE.0006011

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Consolidated OpenCitations Corpus – April 2017

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1 February 2020

2009PLoSO...4.6011R

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Consolidated OpenCitations Corpus – April 2017

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Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

Europe PubMed Central

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1 February 2020

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Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

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