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Abstract

The role of His145 in the T1 copper center of nitrite reductase (NiR) is pivotal for the activity of the enzyme. Mutation to a glycine at this position enables the reconstitution of the T1 center by the addition of imidazole as exogenous ligands, however the catalytic activity is only marginally rescued. Here, we demonstrate that the uptake of 1,3‐dimethylimidazolylidene as N‐heterocyclic carbene (NHC) by the H145G NiR mutant instead of imidazole yields a significantly more active catalyst, suggesting a beneficial role of such C‐bonding. Spectroscopic analyses of the formed H145G≈NHC variant as well as an analogue without the catalytic T2 copper center reveal no significant alteration of the T1 site compared to the wild type or the variant containing imidazole as exogenous N‐bound surrogate of H145. However, the presence of the carbene doubles the catalytic activity of the mutant compared to the imidazole variant. This enhanced activity has been attributed to a faster electron transfer to the T1 center in the NHC variant and a concomitant change of the rate‐limiting step.