http://purl.uniprot.org/citations/8662692 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/8662692 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/8662692 | http://www.w3.org/2000/01/rdf-schema#comment | "There is a common polymorphism in the promoter sequence of the human stromelysin-1 gene, with one allele having a run of six adenosines (6A) and the other five adenosines (5A). We have previously reported, in a 3-year follow-up study of patients with coronary atherosclerosis, that those patients who are homozygous for the 6A allele show a more rapid progression of the disease. In this study, we have investigated whether the 5A/6A promoter polymorphism plays a role in the regulation of stromelysin-1 gene expression. In transient transfection experiments, a stromelysin-1 promoter construct with 6A at the polymorphic site was found to express less of the chloramphenicol acetyltransferase reporter gene than a construct containing 5A. Electrophoretic mobility shift assay and DNase I footprinting revealed the interaction of one or more nuclear protein(s) with the DNA sequence at the 5A/6A polymorphic site. The binding of one of the nucleoprotein factors was more readily detectable with an oligonucleotide probe corresponding to the 6A allele as compared with a probe corresponding to the 5A allele. Replacing the core binding sequence with a random DNA sequence abolished the interaction between the nuclear protein(s) and the probe and also increased reporter gene expression in transiently transfected cells. Thus, the common 5A/6A polymorphism of the human stromelysin-1 promoter appears to play an important role in regulating stromelysin-1 gene expression and may be involved in the progression of coronary heart disease."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.271.22.13055"xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.271.22.13055"xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Ye S."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Ye S."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Humphries S.E."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Humphries S.E."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Eriksson P."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Eriksson P."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Kurkinen M."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Kurkinen M."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Hamsten A."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Hamsten A."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Henney A.M."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/author | "Henney A.M."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/date | "1996"xsd:gYear |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/date | "1996"xsd:gYear |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/name | "J. Biol. Chem."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/name | "J. Biol. Chem."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/pages | "13055-13060"xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/pages | "13055-13060"xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/title | "Progression of coronary atherosclerosis is associated with a common genetic variant of the human stromelysin-1 promoter which results in reduced gene expression."xsd:string |
http://purl.uniprot.org/citations/8662692 | http://purl.uniprot.org/core/title | "Progression of coronary atherosclerosis is associated with a common genetic variant of the human stromelysin-1 promoter which results in reduced gene expression."xsd:string |