Abstract
The flavin adenine dinucleotide-containing domain of the protein MICAL (molecule interacting with CasL) is a monooxygenase. This protein plays an important role in the regulation of axonal guidance. However, the mechanism of this process has been unknown until recently. Only two years ago, F-actin was found to be the physiological substrate. The oxidation of methionine residues of this substrate is catalyzed by MICAL, resulting in the depolymerization of actin. A year ago it was shown that methionine sulfoxide reductase (MSR) catalyzes the reverse reaction of reduction of oxidized actin methionines. Therefore, this couple of proteins is currently a target for manipulation of the ability of neurons to regenerate their axons. The present study deals with different approaches to the regulation of the activity of MICAL and MSR and the design of inhibitors of the former enzyme.
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