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Updated: Sep 6, 2026

Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
Published on: June 21, 2018
Association between PRKG1 gene and gene-environment interactions with pediatric asthma
Jun Liu1,2, Bing Wei1, Yuxuan Zhang1
1Department of Neonatology, General Hospital of Northern Theater Command, Shenyang, P.R. China.
Objective:
To investigate the relationship between single nucleotide polymorphisms (SNPs) of cGMP-dependent protein kinase I (PRKG1) gene and gene-environment interactions with bronchial asthma in children.
Methods:
109 asthma patients and 158 healthy controls from the General Hospital of Northern Theater Command were enrolled, based case-control study. The iMLDR® multiple SNP typing technique was applied to detect the genotypes of rs7903366, rs7081864, rs7070958 and rs7897633 in PRKG1 gene. The percentage of eosinophils (EOS%) in peripheral blood and serum immunoglobulin E (IgE) in the case group were also measured. Gene-environment interactions were examined using the generalized multi-factor dimensionality reduction (GMDR) method.
Results:
There were polymorphisms in four SNPs of PRKG1 gene in the case and control groups. The genotype and allele frequencies distribution of rs7897633 demonstrated statistical significance (p < 0.05). There were no statistically significant differences in EOS% and IgE among genotypes at the four SNPs of PRKG1 gene (p > 0.05). The haplotypes CAGA and TGAC presented significant association with asthma risk (p < 0.05). The four-factor model indicated a potential gene-environment interaction in rs7897633, allergen exposure, residence, and environmental tobacco smoke (ETS) exposure (p < 0.05).
Conclusions:
The rs7897633 in PRKG1 gene was associated with susceptibility to childhood asthma, and C allele is a protective factor. The haplotype CAGA had a protective effect against asthma risk and TGAC was linked to the high risk of developing asthma. Moreover, the interaction of rs7897633, allergen exposure, residence, and ETS exposure conferred susceptibility to childhood asthma.
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