Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 62, Issue 16, Pages 1804-1813Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-005-5098-z
Keywords
myocardial infarction; common disease; single-nucleotide polymorphism (SNP); whole-genome association study; lymphotoxin-alpha (LTA); galectin-2
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Myocardial infarction might result from the interactions of multiple genetic and environmental factors, none of which can cause disease solely by each of themselves. Although molecular biological studies revealed that a number of proteins are possibly involved in its pathogenesis, little, if any genetic findings have been reported so far. To reveal genetic backgrounds of myocardial infarction, we performed a large-scale, case-control association study using 92,788 gene-based single-nucleotide polymorphism (SNP) markers. We have identified functional SNPs within the lymphotoxin-a gene (LTA) located on chromosome 6p21 that conferred susceptibility to myocardial infarction. Furthermore, we could identify galectin-2 protein as a binding partner of LTA protein. The association study further revealed that a functional SNP in LGALS2 encoding galectin-2, which led to altered secretion of LTA, also indicated a risk of myocardial infarction. A combined strategy of genetic and molecular-cellular biological approaches may be useful in clarifying pathogenesis of common diseases.
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