| pubmed-article:16284189 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16284189 | lifeskim:mentions | umls-concept:C1158770 | lld:lifeskim |
| pubmed-article:16284189 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16284189 | pubmed:dateCreated | 2005-11-14 | lld:pubmed |
| pubmed-article:16284189 | pubmed:abstractText | Reactive oxygen species contribute to the pathogenesis of a number of disparate disorders including tissue inflammation, heart failure, hypertension, and atherosclerosis. In response to oxidative stress, cells activate expression of a number of genes, including those required for the detoxification of reactive molecules as well as for the repair and maintenance of cellular homeostasis. In many cases, these induced genes are regulated by transcription factors whose structure, subcellular localization, or affinity for DNA is directly or indirectly regulated by the level of oxidative stress. This review summarizes the recent progress on how cellular redox status can regulate transcription-factor activity and the implications of this regulation for cardiovascular disease. | lld:pubmed |
| pubmed-article:16284189 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16284189 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16284189 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16284189 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16284189 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16284189 | pubmed:issn | 1524-4571 | lld:pubmed |
| pubmed-article:16284189 | pubmed:author | pubmed-author:ColavittiRena... | lld:pubmed |
| pubmed-article:16284189 | pubmed:author | pubmed-author:RoviraIlsa... | lld:pubmed |
| pubmed-article:16284189 | pubmed:author | pubmed-author:FinkelTorenT | lld:pubmed |
| pubmed-article:16284189 | pubmed:author | pubmed-author:LiuHongjunH | lld:pubmed |
| pubmed-article:16284189 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:16284189 | pubmed:day | 11 | lld:pubmed |
| pubmed-article:16284189 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:16284189 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16284189 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16284189 | pubmed:pagination | 967-74 | lld:pubmed |
| pubmed-article:16284189 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16284189 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16284189 | pubmed:articleTitle | Redox-dependent transcriptional regulation. | lld:pubmed |
| pubmed-article:16284189 | pubmed:affiliation | National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. | lld:pubmed |
| pubmed-article:16284189 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16284189 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:16284189 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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