(A) Main splice variants of hIMPDH1: hIMPDH1α (546aa) and hIMPDH1γ (595aa) contain extended sequences at the COOH- terminus (546aa) or both the NH2- and COOH-termini (595aa). (B) S416D mutant recombinant proteins were rigorously normalized to their wildtype counterparts preceding enzymatic analysis. (C) Effect of S416D substitution on the Michaelis-Menten kinetics of hIMPDH1β (514aa); hIMPDH1α (546aa); and hIMPDH1γ (595aa) isoforms. Mutation S416D increased the Km for IMP and decreased the Vmax significantly in hIMPDHα (546aa) and γ (595aa) splice variants, with the effect being maximal in the hIMPDH1α (546aa) isoform. Kinetic parameters were: hIMPDH1β (514aa) [Vmax = 0.099 ± 0.004, Km = 7.62 ± 1.69]; S416D/hIMPDH1β (514aa) [Vmax = 0.084 ± 0.002, Km = 19.13 ± 1.75]; hIMPDH1α (546aa) [Vmax = 0.152 ± 0.002, Km = 20.72 ± 1.32]; S416D/hIMPDH1α (546aa) [Vmax = 0.046 ± 0.002, Km = 59.59 ± 9.74]; hIMPDH1γ (595aa) [Vmax = 0.093 ± 0.003, Km = 12.86 ± 2.18]; S416D/hIMPDH1γ (595aa) [Vmax = 0.049 ± 0.001, Km = 13.95 ± 1.71]. Results represent the media and S.E.M of three independent experiments with three technical replicates each.