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. 2015 Nov 17;59(12):7483–7488. doi: 10.1128/AAC.01804-15

FIG 2.

FIG 2

Molecular representation of the acyl-enzyme complex of CMY-2 (A) and CMY-33 (B) as Connolly surface, with FEP docked in the active site. The model suggests that the reason for increased drug hydrolysis is the ready formation of Michaelis complex (kcat is greater, Km is lower). In particular, two different possible conformations were seen in the widened active site of CMY-33, suggesting the structural basis for resistance in CMY-33 versus CMY-2.