Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1750-1326
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold ; volume:6 ; number:1 ; day:22 ; month:9 ; year:2011 ; pages:1-20 ; date:12.2011
Molecular neurodegeneration ; 6, Heft 1 (22.9.2011), 1-20, 12.2011
- Creator
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Grabrucker, Andreas M.
- Contributor
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Schmeisser, Michael J.
Udvardi, Patrick T.
Arons, Magali
Schoen, Michael
Woodling, Nathaniel S.
Andreasson, Katrin I.
Hof, Patrick R.
Buxbaum, Joseph D.
Garner, Craig C.
Boeckers, Tobias M.
SpringerLink (Online service)
- DOI
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10.1186/1750-1326-6-65
- URN
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urn:nbn:de:1111-2016073068076
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
- 14.08.2025, 11:02 AM CEST
Data provider
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Associated
- Grabrucker, Andreas M.
- Schmeisser, Michael J.
- Udvardi, Patrick T.
- Arons, Magali
- Schoen, Michael
- Woodling, Nathaniel S.
- Andreasson, Katrin I.
- Hof, Patrick R.
- Buxbaum, Joseph D.
- Garner, Craig C.
- Boeckers, Tobias M.
- SpringerLink (Online service)
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Amyloid-beta mediates homeostatic synaptic plasticity
Deletion of the autism-associated protein SHANK3 abolishes structural synaptic plasticity after brain trauma
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Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models
Shank3 deficiency alters midbrain GABAergic neuron morphology, GABAergic markers and synaptic activity in primary striatal neurons
Membrane palmitoylated protein 2 is a synaptic scaffold protein required for synaptic SK2-containing channel function
ProSAP2/Shank3 deficiency abrogates synaptic plasticity after brain trauma
SHANK3 deficiency leads to myelin dysregulation in a Shank3∆11(-/-) mouse model and human iPSC-derived cerebral organoids
Loss of ASD-associated scaffold Shank3 induces dendritic accumulation of pTau
Altered synaptic ultrastructure in the prefrontal cortex of Shank3-deficient rats
Synaptic pathways related to Shank3 and its interaction partner ProSAPiP1
Amyloid-beta mediates homeostatic synaptic plasticity
Deletion of the autism-associated protein SHANK3 abolishes structural synaptic plasticity after brain trauma
Das neuronale Scaffold-Protein Shank3 vermittelt Signaltransduktion und biologische Funktionen der Rezeptor-Tyrosinkinase Ret in Epithelzellen
Das neuronale Scaffold-Protein Shank3 vermittelt Signaltransduktion und biologische Funktionen der Rezeptor-Tyrosinkinase Ret in Epithelzellen
Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models
Shank3 deficiency alters midbrain GABAergic neuron morphology, GABAergic markers and synaptic activity in primary striatal neurons
Membrane palmitoylated protein 2 is a synaptic scaffold protein required for synaptic SK2-containing channel function
ProSAP2/Shank3 deficiency abrogates synaptic plasticity after brain trauma
SHANK3 deficiency leads to myelin dysregulation in a Shank3∆11(-/-) mouse model and human iPSC-derived cerebral organoids
Loss of ASD-associated scaffold Shank3 induces dendritic accumulation of pTau
Altered synaptic ultrastructure in the prefrontal cortex of Shank3-deficient rats
Synaptic pathways related to Shank3 and its interaction partner ProSAPiP1
Amyloid-beta mediates homeostatic synaptic plasticity
Deletion of the autism-associated protein SHANK3 abolishes structural synaptic plasticity after brain trauma
Das neuronale Scaffold-Protein Shank3 vermittelt Signaltransduktion und biologische Funktionen der Rezeptor-Tyrosinkinase Ret in Epithelzellen
Das neuronale Scaffold-Protein Shank3 vermittelt Signaltransduktion und biologische Funktionen der Rezeptor-Tyrosinkinase Ret in Epithelzellen
Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models
Shank3 deficiency alters midbrain GABAergic neuron morphology, GABAergic markers and synaptic activity in primary striatal neurons