PubMed:28490634 / 1263-1659 JSONTXT

{"project":"sentences","denotations":[{"id":"T7","span":{"begin":0,"end":396},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine-induced barrier dysfunction."}

{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":11,"end":18},"obj":"http://purl.obolibrary.org/obo/MAT_0000526"}],"text":"Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine-induced barrier dysfunction."}

{"project":"Inflammaging","denotations":[{"id":"T7","span":{"begin":0,"end":396},"obj":"Sentence"},{"id":"T7","span":{"begin":0,"end":396},"obj":"Sentence"}],"text":"Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine-induced barrier dysfunction."}

{"project":"mondo_disease","denotations":[{"id":"T12","span":{"begin":79,"end":86},"obj":"Disease"}],"attributes":[{"id":"A12","pred":"mondo_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/MONDO_0005292"}],"text":"Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine-induced barrier dysfunction."}

{"project":"HP-phenotype","denotations":[{"id":"T9","span":{"begin":79,"end":86},"obj":"Phenotype"}],"attributes":[{"id":"A9","pred":"hp_id","subj":"T9","obj":"HP:0002583"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine-induced barrier dysfunction."}

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":11,"end":18},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000526"}],"text":"Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine-induced barrier dysfunction."}