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Association study of the Epac gene and tobacco smoking and nicotine dependence
Author(s) -
Chen Xiangning,
Wu Baichai,
Kendler Kenneth S.
Publication year - 2004
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30040
Subject(s) - nicotine , single nucleotide polymorphism , allele , snp , genotype , gene , prefrontal cortex , genetics , nicotine dependence , signal transduction , genetic association , endocrinology , medicine , biology , neuroscience , cognition
Exchange protein directly activated by cAMP (Epac) has been shown to increase its expression in rat prefrontal cortex after self‐administration of nicotine. [Konu et al. 2001: Brain Res 909:194–203]. We investigated the role of the human ortholog of Epac in tobacco smoking and nicotine dependence (ND). Using a case‐control design, we typed 5 SNPs in this gene in 688 subjects, of whom 244 were non‐smokers, 215 were Low‐ND smokers, and 229 were High‐ND smokers. We tested allele and genotype association to smoking initiation (SI) and progression to ND. Three of the five typed SNPs showed modest allele association with progression to ND. Weak association with SI was also observed for one SNP. Considering the function of the gene in cellular signal transduction pathway, its elevated expression after nicotine self‐administration, and multiple markers association with both SI and progression to ND, it is plausible to suggest that variants in Epac contribute to the liability to ND. © 2004 Wiley‐Liss, Inc.