Regulation of synaptic Rac1 activity, long-term potentiation maintenance, and learning and memory by BCR and ABR Rac GPPase-activating proteins

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dc.contributor.authorD Oh-
dc.contributor.authorS Han-
dc.contributor.authorJ Seo-
dc.contributor.authorJae-Ran Lee-
dc.contributor.authorJ Choi-
dc.contributor.authorJ Groffen-
dc.contributor.authorK Kim-
dc.contributor.authorY S Cho-
dc.contributor.authorH S Choi-
dc.contributor.authorH Shin-
dc.contributor.authorJ Woo-
dc.contributor.authorH Won-
dc.contributor.authorS K Park-
dc.contributor.authorS Y Kim-
dc.contributor.authorJ Jo-
dc.contributor.authorD J Whitcomb-
dc.contributor.authorK Cho-
dc.contributor.authorH Kim-
dc.contributor.authorY C Bae-
dc.contributor.authorN Heisterkamp-
dc.contributor.authorS Y Choi-
dc.contributor.authorE Kim-
dc.date.accessioned2017-04-19T09:19:56Z-
dc.date.available2017-04-19T09:19:56Z-
dc.date.issued2010-
dc.identifier.issn02706474-
dc.identifier.uri10.1523/JNEUROSCI.1711-10.2010ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9782-
dc.description.abstractRho family small GTPases are important regulators of neuronal development. Defective Rho regulation causes nervous system dysfunctions including mental retardation and Alzheimer's disease. Rac1, a member of the Rho family, regulates dendritic spines and excitatory synapses, but relatively little is known about how synaptic Rac1 is negatively regulated. Breakpoint cluster region (BCR) is a Rac GTPase-activating protein known to form a fusion protein with the c-Abl tyrosine kinase in Philadelphia chromosome-positive chronic myelogenous leukemia. Despite the fact that BCR mRNAs are abundantly expressed in the brain, the neural functions of BCR protein have remained obscure. We report here that BCR and its close relative active BCR-related (ABR) localize at excitatory synapses and directly interact with PSD-95, an abundant postsynaptic scaffolding protein. Mice deficient for BCR or ABR show enhanced basal Rac1 activity but only a small increase in spine density. Importantly, mice lacking BCR or ABR exhibit a marked decrease in the maintenance, but not induction, of long-term potentiation, and show impaired spatial and object recognition memory. These results suggest that BCR and ABR have novel roles in the regulation of synaptic Rac1 signaling, synaptic plasticity, and learning and memory, and that excessive Rac1 activity negatively affects synaptic and cognitive functions.-
dc.publisherSoc Neuroscience-
dc.titleRegulation of synaptic Rac1 activity, long-term potentiation maintenance, and learning and memory by BCR and ABR Rac GPPase-activating proteins-
dc.title.alternativeRegulation of synaptic Rac1 activity, long-term potentiation maintenance, and learning and memory by BCR and ABR Rac GPPase-activating proteins-
dc.typeArticle-
dc.citation.titleJournal of Neuroscience-
dc.citation.number42-
dc.citation.endPage14144-
dc.citation.startPage14134-
dc.citation.volume30-
dc.contributor.affiliatedAuthorJae-Ran Lee-
dc.contributor.alternativeName오대영-
dc.contributor.alternativeName한승남-
dc.contributor.alternativeName서진수-
dc.contributor.alternativeName이재란-
dc.contributor.alternativeName최정훈-
dc.contributor.alternativeNameGroffen-
dc.contributor.alternativeName김가람-
dc.contributor.alternativeName조이설-
dc.contributor.alternativeName최한샘-
dc.contributor.alternativeName신혜원-
dc.contributor.alternativeName우주연-
dc.contributor.alternativeName원혜정-
dc.contributor.alternativeName박순권-
dc.contributor.alternativeName김수영-
dc.contributor.alternativeName조지훈-
dc.contributor.alternativeNameWhitcomb-
dc.contributor.alternativeName조광욱-
dc.contributor.alternativeName김현-
dc.contributor.alternativeName배용철-
dc.contributor.alternativeNameHeisterkamp-
dc.contributor.alternativeName최세영-
dc.contributor.alternativeName김은준-
dc.identifier.bibliographicCitationJournal of Neuroscience, vol. 30, no. 42, pp. 14134-14144-
dc.identifier.doi10.1523/JNEUROSCI.1711-10.2010-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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