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pubmed-article:12911579 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C0033706 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C0005456 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C1415629 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C1442756 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C0086222 | lld:lifeskim |
pubmed-article:12911579 | lifeskim:mentions | umls-concept:C1149367 | lld:lifeskim |
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pubmed-article:12911579 | lifeskim:mentions | umls-concept:C1705733 | lld:lifeskim |
pubmed-article:12911579 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:12911579 | pubmed:dateCreated | 2003-8-12 | lld:pubmed |
pubmed-article:12911579 | pubmed:abstractText | Prothrombin is a key component in blood coagulation. Overexpression of prothrombin leads to an increased risk of venous thrombosis. Therefore, the study of the transcriptional regulation of the prothrombin gene may help to identify mechanisms of overexpression. | lld:pubmed |
pubmed-article:12911579 | pubmed:language | eng | lld:pubmed |
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pubmed-article:12911579 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12911579 | pubmed:month | Aug | lld:pubmed |
pubmed-article:12911579 | pubmed:issn | 1538-7933 | lld:pubmed |
pubmed-article:12911579 | pubmed:author | pubmed-author:BertinaR MRM | lld:pubmed |
pubmed-article:12911579 | pubmed:author | pubmed-author:RoyD NDN | lld:pubmed |
pubmed-article:12911579 | pubmed:author | pubmed-author:De JongMM | lld:pubmed |
pubmed-article:12911579 | pubmed:author | pubmed-author:CeelieHH | lld:pubmed |
pubmed-article:12911579 | pubmed:author | pubmed-author:Spaargaren-Va... | lld:pubmed |
pubmed-article:12911579 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12911579 | pubmed:volume | 1 | lld:pubmed |
pubmed-article:12911579 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12911579 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12911579 | pubmed:pagination | 1688-98 | lld:pubmed |
pubmed-article:12911579 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:12911579 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12911579 | pubmed:articleTitle | Functional characterization of transcription factor binding sites for HNF1-alpha, HNF3-beta (FOXA2), HNF4-alpha, Sp1 and Sp3 in the human prothrombin gene enhancer. | lld:pubmed |
pubmed-article:12911579 | pubmed:affiliation | Department of Haematology, Leiden University Medical Center, Leiden, the Netherlands. hceelie@lumc.nl | lld:pubmed |
pubmed-article:12911579 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12911579 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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