RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/20421637http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20421637http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20421637http://www.w3.org/2000/01/rdf-schema#comment"Because NF-kappaB signaling pathways are highly conserved in evolution, the fruit fly Drosophila melanogaster provides a good model to study these cascades. We carried out an RNA interference (RNAi)-based genome-wide in vitro reporter assay screen in Drosophila for components of NF-kappaB pathways. We analyzed 16,025 dsRNA-treatments and identified 10 novel NF-kappaB regulators. Of these, nine dsRNA-treatments affect primarily the Toll pathway. G protein-coupled receptor kinase (Gprk)2, CG15737/Toll pathway activation mediating protein, and u-shaped were required for normal Drosomycin response in vivo. Interaction studies revealed that Gprk2 interacts with the Drosophila IkappaB homolog Cactus, but is not required in Cactus degradation, indicating a novel mechanism for NF-kappaB regulation. Morpholino silencing of the zebrafish ortholog of Gprk2 in fish embryos caused impaired cytokine expression after Escherichia coli infection, indicating a conserved role in NF-kappaB signaling. Moreover, small interfering RNA silencing of the human ortholog GRK5 in HeLa cells impaired NF-kappaB reporter activity. Gprk2 RNAi flies are susceptible to infection with Enterococcus faecalis and Gprk2 RNAi rescues Toll(10b)-induced blood cell activation in Drosophila larvae in vivo. We conclude that Gprk2/GRK5 has an evolutionarily conserved role in regulating NF-kappaB signaling."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1000261"xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Hultmark D."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Hultmark D."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Kallio J."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Kallio J."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Ulvila J."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Ulvila J."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Kaustio M."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Kaustio M."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Myllymaki H."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Myllymaki H."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Ramet M."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Ramet M."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Silvennoinen O."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Silvennoinen O."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Valanne S."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Valanne S."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Engstrom Y."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Engstrom Y."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Kleino A."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Kleino A."xsd:string
http://purl.uniprot.org/citations/20421637http://purl.uniprot.org/core/author"Parikka M."xsd:string