Monooxygenase that promotes depolymerization of F-actin by mediating oxidation of specific methionine residues on actin. Acts by modifying actin subunits through the addition of oxygen to form methionine-sulfoxide, leading to promote actin filament severing and prevent repolymerization (Probable). 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. Belongs to the Mical family. 4 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Motility/polarity/chemotaxis; EC 1.14.13.-; Adaptor/scaffold
Molecular Function: actin binding; oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, NADH or NADPH as one donor, and incorporation of one atom of oxygen; protein binding; Rab GTPase binding; SH3 domain binding; zinc ion binding
Biological Process: actin filament depolymerization; cytoskeleton organization and biogenesis; negative regulation of caspase activity; negative regulation of protein amino acid phosphorylation; signal transduction; sulfur oxidation
Alt. Names/Synonyms: CasL interacting molecule; DKFZp434B1517; FLJ11937; FLJ21739; MICA1; MICAL; MICAL-1; MICAL1; microtubule associated monoxygenase, calponin and LIM domain containing 1; Molecule interacting with CasL protein 1; NEDD9 interacting protein with calponin homology and LIM domains; NEDD9-interacting protein with calponin homology and LIM domains; NICAL
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.