| http://purl.uniprot.org/citations/11756486 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11756486 | http://www.w3.org/2000/01/rdf-schema#comment | "The cytokine interleukin-1beta (IL-1beta) contributes to ischemic, excitotoxic, and traumatic brain injury. IL-1beta actions depend on interaction with a single receptor (IL-1RI), which associates with an accessory protein (IL-1RAcP), and is blocked by IL-1 receptor antagonist (IL-1ra). Here we show that in normal mice [wild-type (WT)], intracerebroventricular injection of IL-1ra markedly reduces (-50%; p < 0.01) ischemic brain damage caused by reversible occlusion of the middle cerebral artery, whereas injection of IL-1beta exacerbates damage (+45%; p < 0.05). Mice lacking IL-1RI [IL-1RI knock-out (KO)] exhibited ischemic brain damage that is almost identical to that of the WT (infarct volume 43.7 +/-6.1 and 46.2 +/-6.2 mm3, respectively), but failed to respond to injection of IL-1ra. However, injection of IL-1beta (intracerebroventricularly) exacerbated ischemic brain damage in IL-1RI KO (+61%; p < 0.001) and in WT mice (+45%). This effect of IL-1beta was abolished by heat denaturation in all animals, and was reversed by IL-1ra in WT, but not IL-1RI KO mice. In contrast, IL-1RI KO mice were completely resistant to effects of IL-1beta on food intake or body weight. IL-1RAcP mRNA was increased by stroke in WT, but reduced in IL-1RI KO mice compared with sham-operated mice. Type II IL-1 receptor mRNA was significantly increased 4 hr after ischemia in WT and IL-1RI KO (+20%) animals. These data show that IL-1beta can exacerbate ischemic brain damage independently of IL-1RI and suggest the existence of additional signaling receptor or receptors for IL-1 in the brain."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.org/dc/terms/identifier | "doi:10.1523/jneurosci.22-01-00038.2002"xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "Miller A."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "Parker L."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "Luheshi G."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "Rothwell N."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "Boutin H."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "LeFeuvre R."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/author | "Touzani O."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/name | "J Neurosci"xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/pages | "38-43"xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/title | "Interleukin-1 influences ischemic brain damage in the mouse independently of the interleukin-1 type I receptor."xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://purl.uniprot.org/core/volume | "22"xsd:string |
| http://purl.uniprot.org/citations/11756486 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11756486 |
| http://purl.uniprot.org/citations/11756486 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11756486 |
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| http://purl.uniprot.org/uniprot/#_P13504-mappedCitation-11756486 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11756486 |
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| http://purl.uniprot.org/uniprot/#_Q8C833-mappedCitation-11756486 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11756486 |
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