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Article: PIKE-mediated PI3-kinase activity is required for AMPA receptor surface expression

TitlePIKE-mediated PI3-kinase activity is required for AMPA receptor surface expression
Authors
KeywordsPIKE
PI3K
LTP
GRIP1
GluA2
Issue Date2011
Citation
EMBO Journal, 2011, v. 30, n. 20, p. 4274-4286 How to Cite?
AbstractAMPAR (α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor) is an ion channel involved in the formation of synaptic plasticity. However, the molecular mechanism that couples plasticity stimuli to the trafficking of postsynaptic AMPAR remains poorly understood. Here, we show that PIKE (phosphoinositide 3-kinase enhancer) GTPases regulate neuronal AMPAR activity by promoting GluA2/GRIP1 association. PIKE-L directly interacts with both GluA2 and GRIP1 and forms a tertiary complex upon glycine-induced NMDA receptor activation. PIKE-L is also essential for glycine-induced GluA2-associated PI3K activation. Genetic ablation of PIKE (PIKE -/-) in neurons suppresses GluA2-associated PI3K activation, therefore inhibiting the subsequent surface expression of GluA2 and the formation of long-term potentiation. Our findings suggest that PIKE-L is a critical factor in controlling synaptic AMPAR insertion. © 2011 European Molecular Biology Organization | All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/219873
ISSN
2015 Impact Factor: 9.643
2015 SCImago Journal Rankings: 7.450

 

DC FieldValueLanguage
dc.contributor.authorChan, Chi Bun-
dc.contributor.authorChen, Yongjun-
dc.contributor.authorLiu, Xia-
dc.contributor.authorTang, Xiaoling-
dc.contributor.authorLee, Chi Wai-
dc.contributor.authorMei, Lin-
dc.contributor.authorYe, Keqiang-
dc.date.accessioned2015-09-24T04:44:12Z-
dc.date.available2015-09-24T04:44:12Z-
dc.date.issued2011-
dc.identifier.citationEMBO Journal, 2011, v. 30, n. 20, p. 4274-4286-
dc.identifier.issn0261-4189-
dc.identifier.urihttp://hdl.handle.net/10722/219873-
dc.description.abstractAMPAR (α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor) is an ion channel involved in the formation of synaptic plasticity. However, the molecular mechanism that couples plasticity stimuli to the trafficking of postsynaptic AMPAR remains poorly understood. Here, we show that PIKE (phosphoinositide 3-kinase enhancer) GTPases regulate neuronal AMPAR activity by promoting GluA2/GRIP1 association. PIKE-L directly interacts with both GluA2 and GRIP1 and forms a tertiary complex upon glycine-induced NMDA receptor activation. PIKE-L is also essential for glycine-induced GluA2-associated PI3K activation. Genetic ablation of PIKE (PIKE -/-) in neurons suppresses GluA2-associated PI3K activation, therefore inhibiting the subsequent surface expression of GluA2 and the formation of long-term potentiation. Our findings suggest that PIKE-L is a critical factor in controlling synaptic AMPAR insertion. © 2011 European Molecular Biology Organization | All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofEMBO Journal-
dc.subjectPIKE-
dc.subjectPI3K-
dc.subjectLTP-
dc.subjectGRIP1-
dc.subjectGluA2-
dc.titlePIKE-mediated PI3-kinase activity is required for AMPA receptor surface expression-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1038/emboj.2011.281-
dc.identifier.pmid21847098-
dc.identifier.scopuseid_2-s2.0-80054913696-
dc.identifier.volume30-
dc.identifier.issue20-
dc.identifier.spage4274-
dc.identifier.epage4286-
dc.identifier.eissn1460-2075-

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