| http://purl.uniprot.org/citations/25449573 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25449573 | http://www.w3.org/2000/01/rdf-schema#comment | "Hepatitis B virus X protein (HBx) transactivates multiple transcription factors including nuclear factor-kappa B (NF-κB) that regulates inflammatory-related genes. However, the regulatory mechanism of HBx in NF-κB activation remains largely unknown. This study reports that HBx augments the interleukin-1β (IL-1β)-induced NF-κB activation via interaction with a Toll-like receptor (TLR) adapter protein, ECSIT (evolutionarily conserved signaling intermediate in Toll pathways). GST pull-down and co-immunoprecipitation analyses showed that HBx interacted with ECSIT. Deletion analysis of HBx in a CytoTrap two-hybrid system revealed that the interaction region of HBx for ECSIT was attributed to aa 51-80. Co-transfection of HBx and ECSIT in IL-1β-stimulated cells appeared to activate IKK and IκB signaling pathway as phosphorylation of both IKK α/β and IκBα was increased whereas knockdown of ECSIT or HBxΔ51-80 mutant attenuated the phosphorylation. As a consequence of IκBα degradation, NF-κB was activated as evidenced by increases in NF-κB transcriptional activity and the nuclear translocation of p65 and p50 that resulted in the induction of IL-10. In contrast, knockdown of ECSIT by siRNA or treatment with an NF-κB selective inhibitor (helenalin) abolished the NF-κB activation and IL-10 expression. We conclude that ECSIT appears to be a novel HBx-interacting signal molecule and their interaction is mechanistically important in IL-1β induction of NF-κB activation."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.virusres.2014.10.025"xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/author | "Lin X."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/author | "Lin W.S."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/author | "Lin X.J."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/author | "Liu L.L."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/author | "Chen W.N."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/author | "Jiao B.Y."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/name | "Virus Res"xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/pages | "236-245"xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/title | "Hepatitis B virus X protein increases the IL-1beta-induced NF-kappaB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT)."xsd:string |
| http://purl.uniprot.org/citations/25449573 | http://purl.uniprot.org/core/volume | "195"xsd:string |
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