We began analyzing https://www.nature.com/articles/jhg200113, but it redirected us to https://www.nature.com/articles/jhg200113. The analysis below is for the second page.

Title[redir]:
Amino-acid substitutions in the IKAP gene product significantly increase risk for bronchial asthma in children | Journal of Human Genetics
Description:
The complex etiology of bronchial asthma (BA), one of the most common inflammatory diseases throughout the world, involves a combination of various genetic and environmental factors. A number of investigators have undertaken linkage and association studies to shed light on the genetic background of BA, but the genetic aspects of this disease are still poorly understood. In the course of a project to screen the entire human genome for single nucleotide polymorphisms (SNPs) that might represent useful markers for large-scale association analyses of common diseases and pharmacogenetic traits, we identified six SNPs within the gene encoding I-κB-associated protein (IKAP), a regulator of the NF-κB signal pathway. Most of these SNPs were in linkage disequilibrium with each other. We observed a strong allelic association between BA in childhood and two of the SNP sites, T3214A (Cys1072Ser) and C3473T (Pro1158Leu); P = 0.000004 for T3214A and P = 0.0009 for C3473T. T3214A was also associated with BA in adult patients (P = 0.000002), but C3473T was not (P = 0.056). To confirm the above results, we compared estimated frequencies of haplotypes of the six SNPs between BA patients and controls. We found a strong association between BA in childhood and a specific haplotype, TGAAAT, that involved two amino-acid substitutions (819T, 2295G, 2446A, 2490A, 3214A, and 3473T; P = 0.00004, odds ratio, 2.94; 95% confidence interval [CI], 2.48–3.4). On the other hand, haplotype TACGTC, which differed from the TGAAAT haplotype in the last five nucleotides, was inversely correlated with the BA phenotype (P = 0.002; odds ratio, 9.83; 95% CI, 8.35–11.31). These results indicated that specific variants of the IKAP gene, or a variant in linkage disequilibrium with the TGAAAT haplotype, might be associated with mechanisms responsible for early-onset BA.

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nature, japan, article, content, human, association, cookies, ikap, asthma, genetic, tokyo, privacy, journal, gene, haplotype, open, osaka, data, information, genetics, bronchial, takeoka, diseases, snps, access, university, research, advertising, february, aminoacid, substitutions, children, unoki, onouchi, doi, miyatake, linkage, genome, tgaaat, study, medicine, medical, department, permissions, optional, media, personal, parties, european, policy,

Topics {✒️}

nature portfolio permissions reprints privacy policy nature advertising social media large-scale association analyses gene encoding i-κb nf-κb signal pathway immunology-related genetic associations personal data data protection ikap gene polymorphisms permissions european economic area strong allelic association snp sites privacy amino-acid substitutions entire human genome human genome center explore content similar content ikap gene bronchial asthma journals search log single nucleotide polymorphisms compared estimated frequencies gut inflammatory processes bpd supports abca3 fax +81-3-5449-5433 e-mail accepting optional cookies manage preferences content common inflammatory diseases human genetics strong association early-onset ba 1007/s100380170109 share article cite article takeoka association studies tamari journal specific haplotype haplotype tacgtc tgaaat haplotype journal publish ba phenotype optional cookies article

Schema {🗺️}

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         headline:Amino-acid substitutions in the IKAP gene product significantly increase risk for bronchial asthma in children
         description: The complex etiology of bronchial asthma (BA), one of the most common inflammatory diseases throughout the world, involves a combination of various genetic and environmental factors. A number of investigators have undertaken linkage and association studies to shed light on the genetic background of BA, but the genetic aspects of this disease are still poorly understood. In the course of a project to screen the entire human genome for single nucleotide polymorphisms (SNPs) that might represent useful markers for large-scale association analyses of common diseases and pharmacogenetic traits, we identified six SNPs within the gene encoding I-ÎºB-associated protein (IKAP), a regulator of the NF-ÎºB signal pathway. Most of these SNPs were in linkage disequilibrium with each other. We observed a strong allelic association between BA in childhood and two of the SNP sites, T3214A (Cys1072Ser) and C3473T (Pro1158Leu); P = 0.000004 for T3214A and P = 0.0009 for C3473T. T3214A was also associated with BA in adult patients (P = 0.000002), but C3473T was not (P = 0.056). To confirm the above results, we compared estimated frequencies of haplotypes of the six SNPs between BA patients and controls. We found a strong association between BA in childhood and a specific haplotype, TGAAAT, that involved two amino-acid substitutions (819T, 2295G, 2446A, 2490A, 3214A, and 3473T; P = 0.00004, odds ratio, 2.94; 95% confidence interval [CI], 2.48â3.4). On the other hand, haplotype TACGTC, which differed from the TGAAAT haplotype in the last five nucleotides, was inversely correlated with the BA phenotype (P = 0.002; odds ratio, 9.83; 95% CI, 8.35â11.31). These results indicated that specific variants of the IKAP gene, or a variant in linkage disequilibrium with the TGAAAT haplotype, might be associated with mechanisms responsible for early-onset BA.
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      headline:Amino-acid substitutions in the IKAP gene product significantly increase risk for bronchial asthma in children
      description: The complex etiology of bronchial asthma (BA), one of the most common inflammatory diseases throughout the world, involves a combination of various genetic and environmental factors. A number of investigators have undertaken linkage and association studies to shed light on the genetic background of BA, but the genetic aspects of this disease are still poorly understood. In the course of a project to screen the entire human genome for single nucleotide polymorphisms (SNPs) that might represent useful markers for large-scale association analyses of common diseases and pharmacogenetic traits, we identified six SNPs within the gene encoding I-ÎºB-associated protein (IKAP), a regulator of the NF-ÎºB signal pathway. Most of these SNPs were in linkage disequilibrium with each other. We observed a strong allelic association between BA in childhood and two of the SNP sites, T3214A (Cys1072Ser) and C3473T (Pro1158Leu); P = 0.000004 for T3214A and P = 0.0009 for C3473T. T3214A was also associated with BA in adult patients (P = 0.000002), but C3473T was not (P = 0.056). To confirm the above results, we compared estimated frequencies of haplotypes of the six SNPs between BA patients and controls. We found a strong association between BA in childhood and a specific haplotype, TGAAAT, that involved two amino-acid substitutions (819T, 2295G, 2446A, 2490A, 3214A, and 3473T; P = 0.00004, odds ratio, 2.94; 95% confidence interval [CI], 2.48â3.4). On the other hand, haplotype TACGTC, which differed from the TGAAAT haplotype in the last five nucleotides, was inversely correlated with the BA phenotype (P = 0.002; odds ratio, 9.83; 95% CI, 8.35â11.31). These results indicated that specific variants of the IKAP gene, or a variant in linkage disequilibrium with the TGAAAT haplotype, might be associated with mechanisms responsible for early-onset BA.
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            type:Organization
      name:Y. Nakamura
      affiliation:
            name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected]
            address:
               name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan
               type:PostalAddress
            type:Organization
      name:M. Tamari
      affiliation:
            name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected]
            address:
               name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan
      name:Fourth Department of Internal Medicine, Tokyo Women's Medical University, Tokyo, Japan, Japan
      name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan
      name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan
      name:Department of Pediatric Allergy, Osaka Prefectural Habikino Hospital, Osaka, Japan, Japan
      name:Fifth Department of Internal Medicine, Osaka Prefectural Habikino Hospital, Osaka, Japan, Japan
      name:Miyatake Asthma Clinic, Osaka, Japan, Japan
      name:College of Nursing, University of Shiga, Shiga, Japan, Japan
      name:Division of Genetic Diagnosis, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan, Japan
      name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan
      name:Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tel. +81-3-5449-5372; Fax +81-3-5449-5433 e-mail: [email protected], Japan

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