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http://purl.uniprot.org/citations/14981253http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14981253http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14981253http://www.w3.org/2000/01/rdf-schema#comment"Chronic changes in neural activity trigger a variety of compensatory homeostatic mechanisms by which neurons maintain a normal level of synaptic input. Here we show that chronic activity blockade triggers a compensatory change in the abundance of GLR-1, a Caenorhabditis elegans glutamate receptor. In mutants lacking a voltage-dependent calcium channel (unc-2) or a vesicular glutamate transporter (VGLUT; eat-4), the abundance of GLR-1 in the ventral nerve cord was increased. Similarly, the amplitude of glutamate-evoked currents in ventral cord interneurons was increased in eat-4 VGLUT mutants compared with wild-type controls. The effects of eat-4 VGLUT mutations on GLR-1 abundance in the ventral cord were eliminated in double mutants lacking both the clathrin adaptin protein unc-11 AP180 and eat-4 VGLUT. In contrast, mutations that decreased ubiquitination of GLR-1 did not prevent increased ventral cord abundance of GLR-1 in eat-4 VGLUT mutants. Taken together, our results suggest that GLR-1 is regulated in a homeostatic manner and that this effect depends on clathrin-mediated endocytosis but does not require ubiquitination of GLR-1."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0306156101"xsd:string
http://purl.uniprot.org/citations/14981253http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0306156101"xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Maricq A.V."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Maricq A.V."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Kaplan J.M."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Kaplan J.M."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Grunwald M.E."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Grunwald M.E."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Mellem J.E."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Mellem J.E."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Strutz N."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/author"Strutz N."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/pages"3190-3195"xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/pages"3190-3195"xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/title"Clathrin-mediated endocytosis is required for compensatory regulation of GLR-1 glutamate receptors after activity blockade."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/title"Clathrin-mediated endocytosis is required for compensatory regulation of GLR-1 glutamate receptors after activity blockade."xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/volume"101"xsd:string
http://purl.uniprot.org/citations/14981253http://purl.uniprot.org/core/volume"101"xsd:string