To comprehensively assess the genetic variation in the CRP gene, we utilized a multi-stage approach. (1.) First, Carlson et al.[32] had resequenced the CRP gene in 23 unrelated European-descent individuals (EA) in the Utah/Centre d'Etude du Polymorphisme Humain (CEPH) panel (Coriell Institute for Medical Research, Camden, NJ), and using linkage disequilibrium had selected tagSNPs that summarized the common variation in the CRP gene. The five tagSNPs polymorphic in EAs, included a triallelic 1440C>T>A (rs3091244) and a commonly studied rare 2667G>C. (2.) Additionally, we conducted a comprehensive search of SNPs available in dbSNP (as of August 2005) which were polymorphic in Caucasians and had a minor allele frequency >1%, and resulted in two additional SNPs with low minor allele frequency (MAF) [4362G>C and 5606G>T]. (3.) Finally, the International HapMap Project[33] showed that two tagSNPs [1919A>T and 3872C>T] were sufficient to assess the variation in the gene, and these two were already included in the selected SNPs. The triallelic SNP could not be genotyped using Taqman; however, previous LD analyses[9] showed that SNPs 3872C>T and 5237A>G together serve as a proxy so these two SNPs were used instead.
