A list of the non-synonymous AKR1C1 and AKR1C2 SNPs modeled showing the amino acid change and the predicted and actual effects on enzyme activity, substrate binding, and cofactor binding.

The first five SNPs are from AKR1C2 and the last SNP is from AKR1C1. The SNDs are all from AKR1C2. Actual effects on enzyme activity and substrate binding in AKR1C2 are determined by comparing the experimental values of Vmax and Km for the variant with those of the WT (normal) using data from Table 3 in Takahashi et al.[4]. An asterisk indicates the difference measured by Takahashi et al. did not reach statistical significance and is thus reported here as “no change”. An increase in Km corresponds to the substrate or cofactor being more weakly bound. No experimental data is provided for AKR1C1 or cofactor binding in AKR1C2 as these were not studied. The “predicted” data summarizes our findings in this paper. Cells highlighted in bold-italic indicate where the predictions derived from our modeling agree with the experimental data.