@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix chebi: . @prefix RNA: . @prefix species: . @prefix occursIn: . @prefix pubmed: . @prefix orcid: . sub:Head { this: np:hasAssertion sub:assertion; np:hasProvenance sub:provenance; np:hasPublicationInfo sub:pubinfo; a np:Nanopublication . } sub:assertion { sub:_1 geneProductOf: mgi:88439; a Protein: . sub:_2 geneProductOf: mgi:104798; a RNA: . sub:_3 rdf:object sub:_2; rdf:predicate belv:increases; rdf:subject chebi:6494; a rdf:Statement . sub:_4 occursIn: species:10090; rdf:object sub:_3; rdf:predicate belv:decreases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:lipopolysaccharide) -> r(MGI:Tnf)", "p(MGI:Cntf) -| (a(CHEBI:lipopolysaccharide) -> r(MGI:Tnf))" . } sub:provenance { beldoc: dce:description "Approximately 61,000 statements."; dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved."; dce:title "BEL Framework Large Corpus Document"; pav:authoredBy sub:_6; pav:version "1.4" . sub:_5 prov:value "Ciliary neurotrophic factor (CNTF) inhibits the production of tumor necrosis factor (TNF) in lipopolysaccharide (LPS)-treated mice and protects against LPS lethality when coadministered with its soluble receptor (sCNTFR alpha). Both of these activities are abolished in adrenalectomized (ADX) mice. LPS-induced pulmonary polymorphonuclear neutrophil (PMN) infiltration and nitric oxide (NO) production were also inhibited by CNTF + sCNTFR alpha but not by CNTF alone. sCNTFR alpha did not alter the clearance or tissue distribution of CNTF. Furthermore, CNTF variants coadministered with sCNTFR alpha protected against LPS toxicity in a manner related to their affinity for the beta components of CNTFR. Thus, inhibition of TNF production and protection against LPS lethality by CNTF/sCNTFR alpha require an intact hypothalamus-pituitary-adrenal axis (HPAA) and may be mediated by endogenous glucocorticoids. This protective effect is, at least in part, due to the inhibition of PMN infiltration and NO production, and appears to be mediated by cells displaying only beta-receptor subtypes."; prov:wasQuotedFrom pubmed:9656141 . sub:_6 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:9656141; prov:wasDerivedFrom beldoc:, sub:_5 . } sub:pubinfo { this: dct:created "2014-07-03T14:31:00.077+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }