| pubmed-article:18166353 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18166353 | lifeskim:mentions | umls-concept:C0009319 | lld:lifeskim |
| pubmed-article:18166353 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:18166353 | lifeskim:mentions | umls-concept:C0020364 | lld:lifeskim |
| pubmed-article:18166353 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
| pubmed-article:18166353 | lifeskim:mentions | umls-concept:C1566154 | lld:lifeskim |
| pubmed-article:18166353 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:18166353 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18166353 | pubmed:dateCreated | 2008-1-1 | lld:pubmed |
| pubmed-article:18166353 | pubmed:abstractText | Prolyl and asparaginyl hydroxylases are key oxygen-sensing enzymes that confer hypoxic sensitivity to transcriptional regulatory pathways including the hypoxia inducible factor 1 (HIF-1) and nuclear factor-kappaB (NF-kappaB). Knockout of either HIF-1 or (IKKbeta-dependent) NF-kappaB pathways in intestinal epithelial cells promotes inflammatory disease in murine models of colitis. Both HIF-1 and NF-kappaB pathways are repressed by the action of hydroxylases through the hydroxylation of key regulatory molecules. | lld:pubmed |
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| pubmed-article:18166353 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18166353 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18166353 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18166353 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18166353 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:18166353 | pubmed:issn | 1528-0012 | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:TaylorCormac... | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:FallonPadraic... | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:KeelyStephen... | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:SeeballuckFer... | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:CallananJohn... | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:ManganNiamh... | lld:pubmed |
| pubmed-article:18166353 | pubmed:author | pubmed-author:CumminsEoin... | lld:pubmed |
| pubmed-article:18166353 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18166353 | pubmed:volume | 134 | lld:pubmed |
| pubmed-article:18166353 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18166353 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18166353 | pubmed:pagination | 156-65 | lld:pubmed |
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| pubmed-article:18166353 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18166353 | pubmed:articleTitle | The hydroxylase inhibitor dimethyloxalylglycine is protective in a murine model of colitis. | lld:pubmed |
| pubmed-article:18166353 | pubmed:affiliation | UCD Conway Institute, University College Dublin, Belfield, Dublin, Ireland. | lld:pubmed |
| pubmed-article:18166353 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18166353 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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