RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/24465689http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24465689http://www.w3.org/2000/01/rdf-schema#comment"The transcription factor NF-κB plays a key regulatory role in lymphocyte activation and generation of immune response. Stimulation of T cell receptor (TCR) induces phosphorylation of CARMA1 by PKCθ, resulting in formation of CARMA1-Bcl10-MALT1 (CBM) complex at lipid rafts and subsequently leading to NF-κB activation. While many molecular events leading to NF-κB activation have been reported, it is less understood how this activation is negatively regulated. We performed a cell-based screening for negative regulators of TCR-mediated NF-κB activation, using mutagenesis and complementation cloning strategies. Here we show that casein kinase-2 interacting protein-1 (CKIP-1) suppresses PKCθ-CBM-NF-κB signaling. We found that CKIP-1 interacts with CARMA1 and competes with PKCθ for association. We further confirmed that a PH domain of CKIP-1 is required for association with CARMA1 and its inhibitory effect. CKIP-1 represses NF-κB activity in unstimulated cells, and inhibits NF-κB activation induced by stimulation with PMA or constitutively active PKCθ, but not by stimulation with TNFα. Interestingly, CKIP-1 does not inhibit NF-κB activation induced by CD3/CD28 costimulation, which caused dissociation of CKIP-1 from lipid rafts. These data suggest that CKIP-1 contributes maintenance of a resting state on NF-κB activity or prevents T cells from being activated by inadequate signaling. In conclusion, we demonstrate that CKIP-1 interacts with CARMA1 and has an inhibitory effect on PKCθ-CBM-NF-κB signaling."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0085762"xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Kobayashi M."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Arai Y."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Koyanagi Y."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Shindo K."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Nagata K."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Yamashita K."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Shinohara M."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Io K."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Takaori-Kondo A."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Tada K."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Sakamoto T."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Kadowaki N."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Takiuchi Y."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/author"Iwai F."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/pages"e85762"xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/title"CKIP-1 is an intrinsic negative regulator of T-cell activation through an interaction with CARMA1."xsd:string
http://purl.uniprot.org/citations/24465689http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/24465689http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24465689
http://purl.uniprot.org/citations/24465689http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24465689
http://purl.uniprot.org/uniprot/#_A0A192GQE0-mappedCitation-24465689http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24465689