@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 go: . @prefix RNA: . @prefix mgi: . @prefix geneProductOf: . @prefix obo: . @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: mgi:96437; a RNA: . sub:_2 occursIn: obo:UBERON_0001276, species:10090; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject go:0001696; a rdf:Statement . sub:assertion rdfs:label "bp(GOBP:\"gastric acid secretion\") -> r(MGI:Igfbp2)" . } 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 "20131211" . sub:_3 prov:value "Gastrin, a potent stimulator of gastric acid secretion, primarily targets the acid-secreting parietal cells and histamine-secreting enterochromaffin like (ECL) cells in the stomach. Accordingly, gastrin-deficient (GAS-KO) mice have a severe impairment in acid secretion. The aim of this study was to characterize changes in gene expression in GAS-KO mice to identify gastrin-regulated genes and to gain insight into how gastric cell types are regulated by gastrin and acid secretion. Affymetrix microarray analysis of GAS-KO and wild type mice identified numerous differentially expressed transcripts. The results were compared to GAS-KO mice treated with gastrin to identify genes that were gastrin-responsive. Finally, genes that were primarily changed due to gastrin and not hypochlorhydria were identified by comparison to mice that are deficient in both gastrin and cholecystokinin (GAS/CCK-KO), since these mice have restored basal acid secretion. The data were validated by quantitative reverse transcriptase polymerase chain reaction analysis. Interestingly, a number of inflammatory response genes were induced in GAS-KO mice and normalized in GAS/CCK-KO mice, suggesting that they were increased in response to low gastric acid. Moreover, a number of parietal cell transcripts that were down-regulated in GAS-KO mice were similarly restored in GAS/CCK-KO mice, suggesting that parietal cell changes were also primarily associated with hypochlorhydria. In contrast, ECL cell genes that were markedly down-regulated in GAS-KO mice continued to be reduced in GAS/CCK-KO mice, demonstrating that gastrin coordinately regulates a number of ECL cell genes, including several involved in histamine synthesis and secretion. Key words: parietal cell, enterochromaffin-like (ECL) cell, cholecystokinin (CCK), parathyroid hormone-related protein (Pthlh), inflammation."; prov:wasQuotedFrom pubmed:17105752 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:17105752; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:33:06.772+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }