| http://purl.uniprot.org/citations/10224059 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10224059 | http://www.w3.org/2000/01/rdf-schema#comment | "The innate immune response is an important defense against pathogenic agents. A component of this response is the NF-kappaB-dependent activation of genes encoding inflammatory cytokines such as interleukin-8 (IL-8) and cell adhesion molecules like E-selectin. Members of the serine/threonine innate immune kinase family of proteins have been proposed to mediate the innate immune response. One serine/threonine innate immune kinase family member, the mouse Pelle-like kinase/human interleukin-1 receptor-associated kinase (mPLK/IRAK), has been proposed to play an obligate role in promoting IL-1-mediated inflammation. However, it is currently unknown whether mPLK/IRAK catalytic activity is required for IL-1-dependent NF-kappaB activation. The present study demonstrates that mPLK/IRAK catalytic activity is not required for IL-1-mediated activation of an NF-kappaB-dependent signal. Intriguingly, catalytically inactive mPLK/IRAK inhibits type 1 tumor necrosis factor (TNF) receptor-dependent NF-kappaB activation. The pathway through which mPLK/IRAK mediates this TNF response is TRADD- and TRAF2-independent. Our data suggest that in addition to its role in IL-1 signaling, mPLK/IRAK is a component of a novel signal transduction pathway through which TNF R1 activates NF-kappaB-dependent gene expression."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.274.19.13077"xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Harrington M.A."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Green M."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Goebl M.G."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Mukaida N."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Donner D.B."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/author | "Vig E."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/date | "1999"xsd:gYear |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/pages | "13077-13084"xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/title | "Modulation of tumor necrosis factor and interleukin-1-dependent NF-kappaB activity by mPLK/IRAK."xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://purl.uniprot.org/core/volume | "274"xsd:string |
| http://purl.uniprot.org/citations/10224059 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/10224059 |
| http://purl.uniprot.org/citations/10224059 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/10224059 |
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| http://purl.uniprot.org/uniprot/#_A0A0U5J4W4-mappedCitation-10224059 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/10224059 |
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| http://purl.uniprot.org/uniprot/#_B1AUW6-mappedCitation-10224059 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/10224059 |
| http://purl.uniprot.org/uniprot/#_B1AUW8-mappedCitation-10224059 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/10224059 |
| http://purl.uniprot.org/uniprot/#_B1AUW9-mappedCitation-10224059 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/10224059 |