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http://purl.uniprot.org/citations/22649547http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22649547http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22649547http://www.w3.org/2000/01/rdf-schema#comment"Negative regulation of the NF-κB transcription factor is essential for tissue homeostasis in response to stress and inflammation. NF-κB activity is regulated by a variety of biochemical mechanisms including phosphorylation, acetylation, and ubiquitination. In this study, we provide the first experimental evidence that NF-κB is regulated by SUMOylation, where the RelA subunit of NF-κB is SUMOylated by PIAS3, a member of the PIAS (protein inhibitor of activated STAT) protein family with E3 SUMO ligase activity. PIAS3-mediated NF-κB repression was compromised by either RelA mutant resistant to SUMOylation or PIAS3 mutant defective in SUMOylation. PIAS3-mediated SUMOylation of endogenous RelA was induced by NF-κB activation thus forming a negative regulatory loop. The SUMOylation of endogenous RelA was enhanced in IκBα null as compared with wild type fibroblasts. The RelA SUMOylation was induced by TNFα but not leptomycin B mediated RelA nuclear translocation. Furthermore, RelA mutants defective in DNA binding were not SUMOylated by PIAS3, suggesting that RelA DNA binding is a signal for PIAS3-mediated SUMOylation. These results support a novel negative feedback mechanism for NF-κB regulation by PIAS3-mediated RelA SUMOylation."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0037636"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0037636"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Kulesz-Martin M."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Kulesz-Martin M."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Bridges R."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Bridges R."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Wortham A."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/author"Wortham A."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/name"PLoS ONE"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/name"PLoS ONE"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/pages"E37636"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/pages"E37636"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/title"NF-kappaB repression by PIAS3 mediated RelA SUMOylation."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/title"NF-kappaB repression by PIAS3 mediated RelA SUMOylation."xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/volume"7"xsd:string
http://purl.uniprot.org/citations/22649547http://purl.uniprot.org/core/volume"7"xsd:string
http://purl.uniprot.org/citations/22649547http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22649547
http://purl.uniprot.org/citations/22649547http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22649547
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