Matches in SemOpenAlex for { <https://semopenalex.org/work/W1969805496> ?p ?o ?g. }
- W1969805496 endingPage "14183" @default.
- W1969805496 startingPage "14170" @default.
- W1969805496 abstract "The synaptic toxicity of soluble amyloid-β (Aβ) oligomers plays a critical role in the pathophysiology of Alzheimer9s disease (AD). Here we report that overexpressed α1-takusan, which we previously identified as a protein that enhances synaptic activity via interaction with PSD-95, mitigates oligomeric Aβ-induced synaptic loss. In contrast, takusan knockdown results in enhanced synaptic damage. α1-Takusan interacts with tau either directly or indirectly, and prevents Aβ-induced tau hyperphosphorylation and mitochondrial fragmentation. Deletion analysis identified the second domain (D2) within the takusan protein that is required for PSD-95 clustering and synaptic protection from Aβ. A 51 aa sequence linking D2 to the PDZ-binding C terminus was found to be as effective as full-length takusan in protecting synapses from Aβ-induced damage. Moreover, a sequence containing the D2 from the human protein discs large homolog 5, when linked to a C-terminal PDZ-binding motif, can also increase the clustering of PSD-95 in cortical dendrites. In summary, α1-takusan protects synapses from Aβ-induced insult via interaction with PSD-95 and tau. Thus, takusan-based protein sequences from either mouse or human may be of potential therapeutic benefit in AD." @default.
- W1969805496 created "2016-06-24" @default.
- W1969805496 creator A5000578896 @default.
- W1969805496 creator A5004497226 @default.
- W1969805496 creator A5005321774 @default.
- W1969805496 creator A5010227886 @default.
- W1969805496 creator A5020187973 @default.
- W1969805496 creator A5022404024 @default.
- W1969805496 creator A5061747535 @default.
- W1969805496 creator A5066753734 @default.
- W1969805496 creator A5072481259 @default.
- W1969805496 creator A5074982927 @default.
- W1969805496 creator A5080609124 @default.
- W1969805496 date "2013-08-28" @default.
- W1969805496 modified "2023-10-06" @default.
- W1969805496 title "Synaptic Protein 1-Takusan Mitigates Amyloid- -Induced Synaptic Loss via Interaction with Tau and Postsynaptic Density-95 at Postsynaptic Sites" @default.
- W1969805496 cites W1487695731 @default.
- W1969805496 cites W1513894992 @default.
- W1969805496 cites W1514559719 @default.
- W1969805496 cites W1796802340 @default.
- W1969805496 cites W1925288097 @default.
- W1969805496 cites W1964049915 @default.
- W1969805496 cites W1968553823 @default.
- W1969805496 cites W1968937229 @default.
- W1969805496 cites W1975040221 @default.
- W1969805496 cites W1976602187 @default.
- W1969805496 cites W1984924722 @default.
- W1969805496 cites W1989130535 @default.
- W1969805496 cites W1992496728 @default.
- W1969805496 cites W1993465897 @default.
- W1969805496 cites W2000668585 @default.
- W1969805496 cites W2001261203 @default.
- W1969805496 cites W2007047564 @default.
- W1969805496 cites W2010204822 @default.
- W1969805496 cites W2011335492 @default.
- W1969805496 cites W2018945212 @default.
- W1969805496 cites W2022532556 @default.
- W1969805496 cites W2025561374 @default.
- W1969805496 cites W2030016169 @default.
- W1969805496 cites W2030602441 @default.
- W1969805496 cites W2034286717 @default.
- W1969805496 cites W2041956586 @default.
- W1969805496 cites W2045318822 @default.
- W1969805496 cites W2066390348 @default.
- W1969805496 cites W2071318481 @default.
- W1969805496 cites W2072329091 @default.
- W1969805496 cites W2074052524 @default.
- W1969805496 cites W2075274847 @default.
- W1969805496 cites W2075421841 @default.
- W1969805496 cites W2082871116 @default.
- W1969805496 cites W2085035881 @default.
- W1969805496 cites W2088714934 @default.
- W1969805496 cites W2092586500 @default.
- W1969805496 cites W2092956762 @default.
- W1969805496 cites W2111040212 @default.
- W1969805496 cites W2118516203 @default.
- W1969805496 cites W2120551490 @default.
- W1969805496 cites W2125985978 @default.
- W1969805496 cites W2129839751 @default.
- W1969805496 cites W2135224381 @default.
- W1969805496 cites W2136901555 @default.
- W1969805496 cites W2140323904 @default.
- W1969805496 cites W2158971252 @default.
- W1969805496 cites W2162807572 @default.
- W1969805496 cites W2163916825 @default.
- W1969805496 cites W2167182434 @default.
- W1969805496 cites W2168681379 @default.
- W1969805496 cites W2172204522 @default.
- W1969805496 cites W52278885 @default.
- W1969805496 doi "https://doi.org/10.1523/jneurosci.4646-10.2013" @default.
- W1969805496 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3756761" @default.
- W1969805496 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23986251" @default.
- W1969805496 hasPublicationYear "2013" @default.
- W1969805496 type Work @default.
- W1969805496 sameAs 1969805496 @default.
- W1969805496 citedByCount "17" @default.
- W1969805496 countsByYear W19698054962014 @default.
- W1969805496 countsByYear W19698054962016 @default.
- W1969805496 countsByYear W19698054962017 @default.
- W1969805496 countsByYear W19698054962018 @default.
- W1969805496 countsByYear W19698054962020 @default.
- W1969805496 countsByYear W19698054962021 @default.
- W1969805496 countsByYear W19698054962022 @default.
- W1969805496 countsByYear W19698054962023 @default.
- W1969805496 crossrefType "journal-article" @default.
- W1969805496 hasAuthorship W1969805496A5000578896 @default.
- W1969805496 hasAuthorship W1969805496A5004497226 @default.
- W1969805496 hasAuthorship W1969805496A5005321774 @default.
- W1969805496 hasAuthorship W1969805496A5010227886 @default.
- W1969805496 hasAuthorship W1969805496A5020187973 @default.
- W1969805496 hasAuthorship W1969805496A5022404024 @default.
- W1969805496 hasAuthorship W1969805496A5061747535 @default.
- W1969805496 hasAuthorship W1969805496A5066753734 @default.
- W1969805496 hasAuthorship W1969805496A5072481259 @default.
- W1969805496 hasAuthorship W1969805496A5074982927 @default.
- W1969805496 hasAuthorship W1969805496A5080609124 @default.
- W1969805496 hasBestOaLocation W19698054961 @default.
- W1969805496 hasConcept C154428179 @default.