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Published ahead of print on May 5, 2005, doi:10.1164/rccm.200409-1223OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 2, July 2005, 183-188

A more recent version of this article appeared on July 15, 2005
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Submitted on September 16, 2004
Accepted on April 17, 2005

Positional Identification of an Asthma Susceptibility Gene on Human Chromosome 5q33

Emiko Noguchi1*, Yukako Yokouchi1, Jiang Zhang2, Kazuko Shibuya3, Akira Shibuya3, Makoto Bannai4, Katsushi Tokunaga4, Hitomi Doi4, Mayumi Tamari5, Makiko Shimizu5, Taro Shirakawa5, Masanao Shibasaki6, Kunio Ichikawa7, and Tadao Arinami2

1 Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan; Department of Pediatrics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan, 2 Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan, 3 Department of Immunology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan, 4 Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Bunkyo, Tokyo, Japan, 5 Laboratory of Genetics of Allergic Diseases, RIKEN SNP Research Center, Yokohama, Kanagawa, Japan, 6 Department of Pediatrics, Tsukuba College of Technology, Tsukuba, Ibaraki, Japan, 7 Department of Pediatrics, Tsukuba Medical Center Hospital, Tsukuba, Ibaraki, Japan

* To whom correspondence should be addressed. E-mail: enoguchi{at}md.tsukuba.ac.jp.

Rationale: Asthma is a common respiratory disease with complex genetic components. We previously reported strong evidence for linkage between mite-sensitive asthma and markers on chromosome 5q33. This area of linkage includes a region homologous to a mouse area that contains a locus involved in regulation of airway hyperreactivity. Objective: The aim of the present study is to identify asthma susceptibility genes on chromosome 5q33. Methods and Results: We performed mutation screening and association analyses of genes in the 9.4-Mb human linkage region. Transmission disequilibrium test analysis of 105 polymorphisms in 155 asthmatic families revealed that six polymorphisms in cytoplasmic FMRP interacting protein 2 gene were associated significantly with the development of asthma (p = 0.000075, odds ratio = 5.9). These six polymorphisms were in complete linkage disequilibrium. In real-time quantitative PCR analysis, subjects homozygous for the haplotype overtransmitted to asthma-affected offspring showed significantly increased level of cytoplasmic FMRP interacting protein 2 gene expression in lymphocytes compared with ones heterozygous for the haplotype (p = 0.038). Conclusions: Our data suggest that cytoplasmic FMRP interacting protein 2 are associated with the development of atopic asthma in humans, and that targeting cytoplasmic FMRP interacting protein 2 could be a novel strategy for treating atopic asthma.
Key words: CYFIP2, ITK, TDT, polymorphism




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