[F-actin]-monooxygenase MICAL1

Definition:

Monooxygenase that promotes depolymerization of F-actin by mediating oxidation of specific methionine residues on actin to form methionine-sulfoxide, resulting in actin filament disassembly and preventing repolymerization. In the absence of actin, it also functions as a NADPH oxidase producing H(2)O(2). Acts as a cytoskeletal regulator that connects NEDD9 to intermediate filaments. Also acts as a negative regulator of apoptosis via its interaction with STK38 and STK38L; acts by antagonizing STK38 and STK38L activation by MST1/STK4. Involved in regulation of lamina-specific connectivity in the nervous system such as the development of lamina-restricted hippocampal connections. Through redox regulation of the actin cytoskeleton controls the intracellular distribution of secretory vesicles containing L1/neurofascin/NgCAM family proteins in neurons, thereby regulating their cell surface levels (By similarity). May act as Rab effector protein and play a role in vesicle trafficking.

References:

[1]. Stéphane Frémont, et al. Oxidation of F-actin controls the terminal steps of cytokinesis. Nat Commun. 2017 Feb 23;8:14528. [Content Brief]

[2]. Amrita Rai, et al. bMERB domains are bivalent Rab8 family effectors evolved by gene duplication. Elife. 2016 Aug 23;5:e18675. [Content Brief]

[3]. Heng Wu, et al. The MICALs are a Family of F-actin Dismantling Oxidoreductases Conserved from Drosophila to Humans. Sci Rep. 2018 Jan 17;8(1):937. [Content Brief]

[4]. Daniela Zucchini, et al. Kinetic and spectroscopic characterization of the putative monooxygenase domain of human MICAL-1. Arch Biochem Biophys. 2011 Nov;515(1-2):1-13. [Content Brief]

[5]. Eric F Schmidt, et al. Release of MICAL autoinhibition by semaphorin-plexin signaling promotes interaction with collapsin response mediator protein. J Neurosci. 2008 Feb 27;28(9):2287-97. [Content Brief]

[6]. Teresa Vitali, et al. Properties and catalytic activities of MICAL1, the flavoenzyme involved in cytoskeleton dynamics, and modulation by its CH, LIM and C-terminal domains. Arch Biochem Biophys. 2016 Mar 1;593:24-37. [Content Brief]

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