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http://purl.uniprot.org/citations/17984088http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17984088http://www.w3.org/2000/01/rdf-schema#comment"Restriction of glutamine synthetase to the nervous system is mainly achieved through the mutual function of the glucocorticoid receptor and the neural restrictive silencing factor, NRSF/REST. Glucocorticoids induce glutamine synthetase expression in neural tissues while NRSF/REST represses the hormonal response in non-neural cells. NRSF/REST is a modular protein that contains two independent repression domains, at the N and C termini of the molecule, and is dominantly expressed in nonneural cells. Neural tissues express however splice variants, REST4/5, which contain the repression domain at the N, but not at the C terminus of the molecule. Here we show that full-length NRSF/REST or its C-terminal domain can inhibit almost completely the induction of gene transcription by glucocorticoids. By contrast, the N-terminal domain not only fails to repress the hormonal response but rather stimulates it markedly. The inductive activity of the N-terminal domain is mediated by hBrm, which is recruited to the promoter only in the concomitant presence of GR. Importantly, a similar inductive activity is also exerted by the splice variant REST4. These findings raise the possibility that NRSF/REST exhibits a dual role in regulation of glutamine synthetase. It represses gene induction in nonneural cells and enhances the hormonal response, via its splice variant, in the nervous system."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m707366200"xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Thiel G."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Rousso T."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Vardimon L."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Dror V."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Abramovitz L."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Ben-Dror I."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Blau L."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Granot L."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Landoy E."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/author"Shapira T."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/pages"110-119"xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/title"Dual role of NRSF/REST in activation and repression of the glucocorticoid response."xsd:string
http://purl.uniprot.org/citations/17984088http://purl.uniprot.org/core/volume"283"xsd:string
http://purl.uniprot.org/citations/17984088http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17984088
http://purl.uniprot.org/citations/17984088http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17984088
http://purl.uniprot.org/uniprot/Q13127#attribution-195C885575E79BB84CD1F246F47E7BDChttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17984088
http://purl.uniprot.org/uniprot/P51531#attribution-195C885575E79BB84CD1F246F47E7BDChttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17984088