@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 chebi: . @prefix RNA: . @prefix hgnc: . @prefix geneProductOf: . @prefix mesh: . @prefix occursIn: . @prefix species: . @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: hgnc:26148; a RNA: . sub:_2 occursIn: mesh:D009000, species:9606; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject chebi:7583; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:\"nitric oxide\") -> r(HGNC:CRTC3)" . } 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:_4; pav:version "1.4" . sub:_3 prov:value "Nitric oxide (NO*) can stabilize mRNA by activating p38 mitogen-activated protein kinase (MAPK). Here, transcript stabilization by NO* was investigated in human THP-1 cells using microarrays. After LPS pre-stimulation, cells were treated with actinomycin D and then exposed to NO* without or with the p38 MAPK inhibitor SB202190 (SB). The decay of 220 mRNAs was affected; most were stabilized by NO*. Unexpectedly, SB often enhanced rather than antagonized transcript stability. NO* activated p38 MAPK and Erk1/2; SB blocked p38 MAPK, but further activated Erk1/2. RT-PCR confirmed that NO* and SB could additively stabilize certain mRNA transcripts, an effect abolished by Erk1/2 inhibition. In affected genes, these responses were associated with CU-rich elements (CURE) in 3'-untranslated regions (3'-UTR). NO* stabilized the mRNA of a CURE-containing reporter gene, while repressing translation. Dominant-negative Mek1, an Erk1/2 inhibitor, abolished this effect. NO* similarly stabilized, but blocked translation of MAP3K7IP2, a natural CURE-containing gene. NO* increased hnRNP translocation to the cytoplasm and binding to CURE. Over-expression of hnRNP K, like NO*, repressed translation of CURE-containing mRNA. These findings define a sequence-specific mechanism of NO*-triggered gene regulation that stabilizes mRNA, but represses translation."; prov:wasQuotedFrom pubmed:16757573 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:16757573; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:43.411+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }