Genome scan for loci linked to mite sensitivity: the Collaborative Study on the Genetics of Asthma (CSGA)

Mn, Blumenthal; Ober, Carole; Beaty, TH; Bleecker, ER; Cd, Langefeld; King, RA; Lester, Lucille A.; Cox, Nancy J.; Barnes, Kathleen C.; Togias, Alkis; Mathias, Rasika A.; Meyers, DA; Oetting, William S.; Rich, Stephen S.

doi:10.1038/sj.gene.6364063

Cited by 38 publications

(22 citation statements)

References 20 publications

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“…The 3p24-p14 region has been reported for atopic dermatitis in a Swedish population, 29 asthma and BHR in the Hutterite population 14,30 and mite sensitivity in the CSGA families. 31 The 9q22-q34 region has been reported for asthma in the Hutterites, 14 for IgE and atopy in the German scan 25 and the region 11p14 for SPT and IgE in the Hutterite population, 14,32 in the first EGEA scan 15 and in the German scan. 25 Finally, the last region detected here for rhinitis, 13q32-qter, has been already reported for asthma in the CSGA sample 22 and for Dermatophagoides pteronyssinus-specific IgE responsiveness 23 in Caucasian CSGA subjects.…”

Section: Discussionmentioning

confidence: 99%

Genome screen in the French EGEA study: detection of linked regions shared or not shared by allergic rhinitis and asthma

et al. 2005

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In the sample of 295 French EGEA families with at least one asthmatic subject, a genome screen was conducted to identify potential linkage regions specific either to allergic rhinitis (AR) or to asthma as well as those shared by the two diseases. Two binary rhinitis phenotypes based on (1) diagnosis (AR bin1 ) and (2) symptoms (AR bin2 ) and a categorical ordered trait (AR cat ) were considered. Asthma phenotype was based on answers to a standardized questionnaire plus the presence of bronchial hyper-responsiveness. Linkage analyses were conducted using the maximum likelihood binomial (MLB) method. These analyses provided potential evidence for linkage to three regions in the whole sample: 1p31 for the phenotype defined by AR bin2 plus asthma (P ¼ 0.00016), 2q32 for AR bin2 (P ¼ 0.00016) and 3p24-p14 for AR cat (P ¼ 0.001). Two other regions were detected in the subset of 185 families with at most one asthmatic sib: 9p22 and 9q22-q34 for AR bin1 (P ¼ 0.001 and 0.0007, respectively). No region showed evidence for linkage to asthma without being also linked to AR. While 1p31 may contain a genetic determinant common to asthma and AR, 2q32, 3p24-p14, 9p22 and 9q22-q34 are more likely to harbor genetic factors specific to AR. Genes and Immunity (2005) 6, 95-102.

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Section: Discussionmentioning

confidence: 99%

Genome screen in the French EGEA study: detection of linked regions shared or not shared by allergic rhinitis and asthma

et al. 2005

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“…25 Chromosomal regions containing the human C3 gene have also been previously linked with asthma and allergic disease in several different human populations. [16][17][18] Moreover, recent findings in a Japanese population implicated both a high-risk and a low-risk SNP haplotype in C3 for bronchial asthma. 19 Taken together, these data provide strong support for C3 as an asthma candidate gene.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, linkage studies on asthma and allergic disease have implicated a region on chromosome 19p, where the gene encoding C3 is located, [16][17][18] and a recent study in a Japanese population supported an association between a single C3 variant and a four-single nucleotide polymorphism (SNP) haplotype and bronchial asthma. 19 The C3 gene covers 42.78 kb, from position 6 628 878 to 6 671 660 (NCBI build 35, February 10, 2005) on the reverse strand, and consists of 41 exons.…”

Section: Introductionmentioning

confidence: 99%

Variants in the gene encoding C3 are associated with asthma and related phenotypes among African Caribbean families

et al. 2005

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Proinflammatory and immunoregulatory products from C3 play a major role in phagocytosis, respiratory burst, and airways inflammation. C3 is critical in adaptive immunity; studies in mice deficient in C3 demonstrate that features of asthma are significantly attenuated in the absence of C3. To test the hypothesis that the C3 gene on chromosome 19p13.3-p13.2 contains variants associated with asthma and related phenotypes, we genotyped 25 single nucleotide polymorphism (SNP) markers distributed at intervals of B1.9 kb within the C3 gene in 852 African Caribbean subjects from 125 nuclear and extended pedigrees. We used the multiallelic test in the family-based association test program to examine sliding windows comprised of 2-6 SNPs. A five-SNP window between markers rs10402876 and rs366510 provided strongest evidence for linkage in the presence of linkage disequilibrium for asthma, high log[total IgE], and high log[IL-13]/[log[IFN-g] in terms of global P-values (P ¼ 0.00027, 0.00013, and 0.003, respectively). A three-SNP haplotype GGC for the first three of these markers showed best overall significance for the three phenotypes (P ¼ 0.003, 0.007, 0.018, respectively) considering haplotype-specific tests. Taken together, these results implicate the C3 gene as a priority candidate controlling risk for asthma and allergic disease in this population of African descent.

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“…It is important to note that the human CC16 gene maps to an important genetic region (11q12-13), which has been linked to asthma and its related phenotypes in studies carried out in various populations (Blumenthal et al 2004;Huang et al 2003;Simon Thomas et al 2000;Young et al 1992). In addition to CC16, several other important candidate genes for asthma, such as Fce RIb, CD20, and Glutathione S-transferase pi (GSTP1) are also localized in this region (Mansur et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Association of an intragenic microsatellite marker in the CC16 gene with asthma in the Indian population

Sharma

Ghosh

2004

J Hum Genet

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The gene for Clara cell secretory protein (CC16) is an ideal candidate for investigating genetic predisposition to asthma because of its role in the airway as an antiinflammatory molecule, differences in its levels between asthmatics and healthy controls, and its genetic location (11q13). We investigated the association of an SNP (A38G) and an intragenic repeat polymorphism in the CC16 gene with asthma and its associated traits, such as total serum IgE levels, in a case control as well as in a family based study design. A significant association was observed for the microsatellite repeat at the level of alleles and genotypes with asthma (P<0.05) in both the study designs. However, no association was observed for the A38G SNP with asthma. When haplotypes were constructed for these two loci and compared, the haplotype A_18 was found at higher frequency in patients (OR=1.59, 95%CI=1.08, 2.33, P=0.016). Also, in the family based design, a biased transmission was observed for haplotypes from parents to affected offspring (P=0.003). Individually, haplotype A_18 showed preferential transmission (82.6%) to affected offspring (P=0.001), thereby confirming the case-control results. In summary, this is the first study identifying the CC16 gene to be associated with asthma in the Indian population.

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Genome scan for loci linked to mite sensitivity: the Collaborative Study on the Genetics of Asthma (CSGA)

Cited by 38 publications

References 20 publications

Genome screen in the French EGEA study: detection of linked regions shared or not shared by allergic rhinitis and asthma

Genome screen in the French EGEA study: detection of linked regions shared or not shared by allergic rhinitis and asthma

Variants in the gene encoding C3 are associated with asthma and related phenotypes among African Caribbean families

Association of an intragenic microsatellite marker in the CC16 gene with asthma in the Indian population

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