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nature portfolio permissions reprints privacy policy gov/snp/index open reading frames advertising nature 349 nature 429 nature jp/research/db/tfsearchj sequence-specific post-transcriptional regulators social media case-control association study author information authors case-control association studies development 121 transcend biotin-lysyl-trna basic gt/ag rule full-length cdna isolation full-length cdna sequence 5× tris–borate-edta buffer author correspondence full-length cdna sequences electrophoretic mobility-shift assay organic anion-transporting polypeptides miat full-length cdna adding digoxigenin-labeled oligonucleotide snp research center large-scale study genome-wide association studies cardiomyocyte-restricted miat deletion northern blot analyses genome-wide tag snps genome-wide snp analysis permissions shattuck lecture-cardiovascular medicine single pcr-amplified product a-allele oligonucleotide bound full-length cdna genome-wide association haplotype analyses revealed similar content coronary heart disease table 2 association analyses table 4 association analyses chemiluminescent detection system pcr-amplified variant product gene-based snp discovery vitro translation assay pre-incubated nuclear extract

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         headline:Identification of a novel non-coding RNA, MIAT, that confers risk of myocardial infarction
         description:Through a large-scale case-control association study using 52,608 haplotype-based single nucleotide polymorphism (SNP) markers, we identified a susceptible locus for myocardial infarction (MI) on chromosome 22q12.1. Following linkage disequilibrium (LD) mapping, haplotype analyses revealed that six SNPs in this locus, all of which were in complete LD, showed markedly significant association with MI (χ 2=25.27, P=0.0000005; comparison of allele frequency, 3,435 affected individuals versus 3,774 controls, in the case of intron 1 5,338 C>T; rs2331291). Within this locus, we isolated a complete cDNA of a novel gene, designated myocardial infarction associated transcript (MIAT). MIAT has five exons, and in vitro translation assay showed that MIAT did not encode any translational product, indicating that this is likely to be a functional RNA. In vitro functional analyses revealed that the minor variant of one SNP in exon 5 increased transcriptional level of the novel gene. Moreover, unidentified nuclear protein(s) bound more intensely to risk allele than non-risk allele. These results indicate that the altered expression of MIAT by the SNP may play some role in the pathogenesis of MI.
         datePublished:2006-12-01T00:00:00Z
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            Myocardial infaraction associated transcript
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            Human Genetics
            Molecular Medicine
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            Gene Therapy
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      headline:Identification of a novel non-coding RNA, MIAT, that confers risk of myocardial infarction
      description:Through a large-scale case-control association study using 52,608 haplotype-based single nucleotide polymorphism (SNP) markers, we identified a susceptible locus for myocardial infarction (MI) on chromosome 22q12.1. Following linkage disequilibrium (LD) mapping, haplotype analyses revealed that six SNPs in this locus, all of which were in complete LD, showed markedly significant association with MI (χ 2=25.27, P=0.0000005; comparison of allele frequency, 3,435 affected individuals versus 3,774 controls, in the case of intron 1 5,338 C>T; rs2331291). Within this locus, we isolated a complete cDNA of a novel gene, designated myocardial infarction associated transcript (MIAT). MIAT has five exons, and in vitro translation assay showed that MIAT did not encode any translational product, indicating that this is likely to be a functional RNA. In vitro functional analyses revealed that the minor variant of one SNP in exon 5 increased transcriptional level of the novel gene. Moreover, unidentified nuclear protein(s) bound more intensely to risk allele than non-risk allele. These results indicate that the altered expression of MIAT by the SNP may play some role in the pathogenesis of MI.
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         Human Genetics
         Molecular Medicine
         Gene Function
         Gene Expression
         Gene Therapy
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      name:Laboratory for Cardiovascular Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan

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