| http://purl.uniprot.org/citations/22331027 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22331027 | http://www.w3.org/2000/01/rdf-schema#comment | "The nuclear factor (NF)-κB family of transcription factors regulates diverse cellular functions, including inflammation, oncogenesis and apoptosis. It was reported that A20 plays a critical role in the termination of NF-κB signaling after activation. Previously, we showed that Ymer interacts and collaborates with A20, followed by degradation of receptor-interacting protein (RIP) and attenuation of NF-κB signaling. Here we show the function of Ymer in regulation of several signaling pathways including NF-κB on the basis of results obtained by using Ymer transgenic (Ymer Tg) mice. Ymer Tg mice exhibited impaired immune responses, including NF-κB and mitogen-activated protein kinase (MAPK) activation, cell proliferation and cytokine production, to tumor necrosis factor (TNF)-α, polyI:C or lipopolysaccharide (LPS) stimulation. Ymer Tg mice were more resistant to LPS-induced septic shock than wild-type mice. Transgene of Ymer inhibited the onset of glomerulonephritis in lpr/lpr mice as an autoimmune disease model. In contrast to the inflammatory immune response to LPS, Fas-mediated cell death was strongly induced in liver cells of Ymer Tg mice in which Ymer is abundantly expressed. These findings suggest that Ymer acts as a regulator downstream of several receptors and that Ymer functions as a positive or negative regulator in a signaling pathway-dependent manner."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.org/dc/terms/identifier | "doi:10.2119/molmed.2011.00435"xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/author | "Tanaka S."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/author | "Tsukiyama T."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/author | "Bohgaki M."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/author | "Hatakeyama S."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/author | "Terai S."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/author | "Matsuda-Tsukiyama M."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/name | "Mol Med"xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/pages | "587-597"xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/title | "Ymer acts as a multifunctional regulator in nuclear factor-kappaB and Fas signaling pathways."xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://purl.uniprot.org/core/volume | "18"xsd:string |
| http://purl.uniprot.org/citations/22331027 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22331027 |
| http://purl.uniprot.org/citations/22331027 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22331027 |
| http://purl.uniprot.org/uniprot/#_Q8IVM0-mappedCitation-22331027 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22331027 |
| http://purl.uniprot.org/uniprot/Q8IVM0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/22331027 |