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| pubmed-article:15341739 | lifeskim:mentions | umls-concept:C1366358 | lld:lifeskim |
| pubmed-article:15341739 | lifeskim:mentions | umls-concept:C0332479 | lld:lifeskim |
| pubmed-article:15341739 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:15341739 | lifeskim:mentions | umls-concept:C2347644 | lld:lifeskim |
| pubmed-article:15341739 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:15341739 | pubmed:dateCreated | 2004-9-2 | lld:pubmed |
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| pubmed-article:15341739 | pubmed:abstractText | The evolutionary forces of mutation, natural selection, and genetic drift shape the pattern of phenotypic variation in nature, but the roles of these forces in defining the distributions of particular traits have been hard to disentangle. To better understand the mechanisms contributing to common variation in humans, we investigated the evolutionary history of a functional polymorphism in the upstream regulatory region of the MMP3 gene. This single base pair insertion/deletion variant, which results in a run of either 5 or 6 thymidines 1608 bp from the transcription start site, alters transcription factor binding and influences levels of MMP3 mRNA and protein. The polymorphism contributes to variation in arterial traits and to the risk of coronary heart disease and its progression. | lld:pubmed |
| pubmed-article:15341739 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15341739 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341739 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15341739 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15341739 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15341739 | pubmed:issn | 0960-9822 | lld:pubmed |
| pubmed-article:15341739 | pubmed:author | pubmed-author:WrayGregory... | lld:pubmed |
| pubmed-article:15341739 | pubmed:author | pubmed-author:RockmanMatthe... | lld:pubmed |
| pubmed-article:15341739 | pubmed:author | pubmed-author:GoldsteinDavi... | lld:pubmed |
| pubmed-article:15341739 | pubmed:author | pubmed-author:HahnMatthew... | lld:pubmed |
| pubmed-article:15341739 | pubmed:author | pubmed-author:SoranzoNicole... | lld:pubmed |
| pubmed-article:15341739 | pubmed:author | pubmed-author:LoiselDagan... | lld:pubmed |
| pubmed-article:15341739 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15341739 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:15341739 | pubmed:volume | 14 | lld:pubmed |
| pubmed-article:15341739 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15341739 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15341739 | pubmed:pagination | 1531-9 | lld:pubmed |
| pubmed-article:15341739 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15341739 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15341739 | pubmed:articleTitle | Positive selection on MMP3 regulation has shaped heart disease risk. | lld:pubmed |
| pubmed-article:15341739 | pubmed:affiliation | Department of Biology, Duke University, Box 90338, Durham, NC 27708, USA. mrockan@duke.edu | lld:pubmed |
| pubmed-article:15341739 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15341739 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15341739 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:15341739 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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