Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2004-9-2
pubmed:databankReference
http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541459, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541460, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541461, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541462, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541463, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541464, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541465, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541466, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541467, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541468, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541469, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541470, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541471, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541472, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541473, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541474, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AY541475
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0960-9822
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1531-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15341739-Animals, pubmed-meshheading:15341739-Base Sequence, pubmed-meshheading:15341739-Coronary Artery Disease, pubmed-meshheading:15341739-DNA Primers, pubmed-meshheading:15341739-Evolution, Molecular, pubmed-meshheading:15341739-Gene Expression Regulation, pubmed-meshheading:15341739-Genetics, Population, pubmed-meshheading:15341739-Haplotypes, pubmed-meshheading:15341739-Humans, pubmed-meshheading:15341739-Likelihood Functions, pubmed-meshheading:15341739-Matrix Metalloproteinase 3, pubmed-meshheading:15341739-Models, Genetic, pubmed-meshheading:15341739-Molecular Sequence Data, pubmed-meshheading:15341739-Mutation, pubmed-meshheading:15341739-Phenotype, pubmed-meshheading:15341739-Phylogeny, pubmed-meshheading:15341739-Polymorphism, Genetic, pubmed-meshheading:15341739-Primates, pubmed-meshheading:15341739-Selection, Genetic, pubmed-meshheading:15341739-Sequence Analysis, DNA
pubmed:year
2004
pubmed:articleTitle
Positive selection on MMP3 regulation has shaped heart disease risk.
pubmed:affiliation
Department of Biology, Duke University, Box 90338, Durham, NC 27708, USA. mrockan@duke.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't