pubmed-article:18323529 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C0030054 | lld:lifeskim |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C0162574 | lld:lifeskim |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C0871712 | lld:lifeskim |
pubmed-article:18323529 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
pubmed-article:18323529 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:18323529 | pubmed:dateCreated | 2008-4-25 | lld:pubmed |
pubmed-article:18323529 | pubmed:abstractText | Myocardial infarction, stroke, and venous thromboembolism are characterized by oxygen deprivation. In hypoxia, biological responses are activated that evoke tissue damage. Rapid activation of early growth response-1 in hypoxia upregulates fundamental inflammatory and prothrombotic stress genes. We probed the mechanisms mediating regulation of early growth response-1 and demonstrate that hypoxia stimulates brisk generation of advanced glycation end products (AGEs) by endothelial cells. Via AGE interaction with their chief signaling receptor, RAGE, membrane translocation of protein kinase C-betaII occurs, provoking phosphorylation of c-Jun NH(2)-terminal kinase and increased transcription of early growth response-1 and its downstream target genes. These findings identify RAGE as a master regulator of tissue stress elicited by hypoxia and highlight this receptor as a central therapeutic target to suppress the tissue injury-provoking effects of oxygen deprivation. | lld:pubmed |
pubmed-article:18323529 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18323529 | pubmed:language | eng | lld:pubmed |
pubmed-article:18323529 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18323529 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:18323529 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18323529 | pubmed:month | Apr | lld:pubmed |
pubmed-article:18323529 | pubmed:issn | 1524-4571 | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:WendtThoralfT | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:SchmidtAnn... | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:KAYL MLM | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:YanShi-FangSF | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:ZouYu ShanYS | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:KongLinghuaL | lld:pubmed |
pubmed-article:18323529 | pubmed:author | pubmed-author:ChangJong... | lld:pubmed |
pubmed-article:18323529 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18323529 | pubmed:day | 25 | lld:pubmed |
pubmed-article:18323529 | pubmed:volume | 102 | lld:pubmed |
pubmed-article:18323529 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18323529 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18323529 | pubmed:pagination | 905-13 | lld:pubmed |
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pubmed-article:18323529 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18323529 | pubmed:articleTitle | Oxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end products. | lld:pubmed |
pubmed-article:18323529 | pubmed:affiliation | Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA. | lld:pubmed |
pubmed-article:18323529 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18323529 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:18323529 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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