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Microtubule associated monooxygenase, calponin and LIM domain containing 2 (MICAL2)

Target
MICAL2
Molecular classification
Enzyme (monooxygenase, specifically flavoprotein monooxygenase), Cytoskeletal protein regulator
01

Overview

Microtubule associated monooxygenase, calponin and LIM domain containing 2 (MICAL2) is a multidomain enzyme with a flavoprotein monooxygenase (MO) domain, calponin homology (CH) domain, and LIM domain[2][3][4]. It serves a crucial role in cytoskeletal dynamics by catalyzing NADPH-dependent oxidation of specific methionine residues (Met-44 and Met-47) on F-actin, resulting in actin filament severing and preventing repolymerization[1][4][2]. MICAL2 also regulates nuclear actin and thus transcriptional activity via the SRF/MRTF-A pathway[4][3]. Increased expression is tightly linked to progression, invasion, and migration of several cancers, likely due to its ability to induce epithelial-mesenchymal transition (EMT)[5][2]. MICAL2 is also involved in myogenic lineage commitment, muscle differentiation, and cytoskeletal homeostasis[1]. Its activity produces reactive oxygen species (ROS), which further drive cytoskeletal rearrangements and can promote oncogenic signaling[2]. MICAL2 represents a potential therapeutic target in oncology and muscle pathologies, and its expression is considered a biomarker for aggressive and metastatic disease[5][4][1].

Other names
[F-actin]-monooxygenase MICAL2KIAA0750MICAL2PV1MICAL2PV2MICALCLMical-cLMICAL-2FLJ14966MICAL C-terminal-like proteinMolecule interacting with CasL protein 2Ebitein1ERK2-binding testicular protein 1[F-actin]-methionine sulfoxide oxidase MICAL2ebitein-1flavoprotein oxidoreductase MICAL2protein-methionine sulfoxide oxidase MICAL2
02

Biological functions

F-actin depolymerization and cytoskeletal dynamicsCell motility and migration (by actin modulation)Regulation of gene transcription (SRF/MRTF-A pathway)Epithelial to mesenchymal transition (EMT; cancer progression)Myogenic lineage commitment and muscle differentiationRegulation of reactive oxygen species (ROS) levels
03

Disease associations

Cancer (gastric, kidney, generally metastasis and invasion)Muscular dystrophies (implicated in disease evolution in DMD)Fraser Syndrome 1
04

Safety considerations

Overexpression promotes cancer cell migration and metastasis, suggesting possible oncogenic potentialTargeting may affect cytoskeletal integrity and muscle function
05

Biomarkers

Overexpression in poorly differentiated and metastatic cancers (prognostic marker)Expression during muscle regeneration and differentiation

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