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Association of the hCLCA1 gene with childhood and adult asthma.

Authors: Kamada, F  Suzuki, Y  Shao, C  Tamari, M  Hasegawa, K  Hirota, T  Shimizu, M  Takahashi, N  Mao, XQ  Doi, S  Fujiwara, H  Miyatake, A  Fujita, K  Chiba, Y  Aoki, Y  Kure, S  Tamura, G  Shirakawa, T  Matsubara, Y 
Citation: Kamada F, etal., Genes Immun. 2004 Nov;5(7):540-7.
Pubmed: (View Article at PubMed) PMID:15318163
DOI: Full-text: DOI:10.1038/sj.gene.6364124

Asthma is caused by bronchial inflammation. This inflammation involves mucus overproduction and hypersecretion. Recently, a mouse model of asthma showed that gob-5 is involved in the pathogenesis of asthma. The gob-5 gene is involved in mucus secretion and its expression is upregulated upon antigen attack in sensitized mice. The observation suggests that human homologue of gob-5, hCLCA1 (human calcium-dependent chloride channel-1), may be involved in human disease. We screened for single-nucleotide polymorphisms (SNPs) in hCLCA1 in the Japanese population. We identified eight SNPs, and performed association studies using 384 child patients with asthma, 480 adult patients with asthma, and 672 controls. In haplotype analysis, we found a different haplotype distribution pattern between controls and childhood asthma (P<0.0001) and between controls and adult asthma (P=0.0031). We identified a high-risk haplotype (CATCAAGT haplotype; P=0.0014) and a low-risk haplotype (TGCCAAGT haplotype; P=0.00010) in cases of childhood asthma. In diplotype analysis, patients who had the CATCAAGT haplotype showed a higher risk for childhood asthma than those who did not (P=0.0011). Individuals who had the TGCCAAGT haplotype showed a lower risk for childhood asthma than those who did not (P<0.0001). Our data suggested that variation of the hCLCA1 gene affects patients' susceptibility for asthma.


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CRRD Object Information
CRRD ID: 4145656
Created: 2010-11-11
Species: All species
Last Modified: 2010-11-11
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.