ReviewInternational journal of molecular sciences2013
MICAL, the flavoenzyme participating in cytoskeleton dynamics.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Prevalence and Functional Roles of Intrinsic Disorder in the [F-actin]-monooxygenase MICAL Family Members and their Interactors.Cell biochemistry and biophysics · 2026Article
- Trem2-MICAL1-P-ERK Axis in Macrophages Confers Protection AgainstPathogens (Basel, Switzerland) · 2025Article
- The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.Human cell · 2025Review
- Autoinhibition and relief mechanisms for MICAL monooxygenases in F-actin disassembly.Nature communications · 2024Article
- Mitochondrial dysfunction as a target in spinal cord injury: intimate correlation between pathological processes and therapeutic approaches.Neural regeneration research · 2023Review
- Actin Bundles Dynamics and Architecture.Biomolecules · 2023Review
- Prognostic impact of MICALL1 and associates with immune infiltration in liver hepatocellular carcinoma patients.Cancer biomarkers : section A of Disease markers · 2023Article
- Magnetic field effects in biology from the perspective of the radical pair mechanism.Journal of the Royal Society, Interface · 2022Review
- Article
- Mitochondria-actin cytoskeleton crosstalk in cell migration.Journal of cellular physiology · 2022Review
- MICAL2 Contributes to Gastric Cancer Cell Proliferation by Promoting YAP Dephosphorylation and Nuclear Translocation.Oxidative medicine and cellular longevity · 2021Article
- Article
- The structure of N184K amyloidogenic variant of gelsolin highlights the role of the H-bond network for protein stability and aggregation properties.European biophysics journal : EBJ · 2020Article
- Deletion of Semaphorin 3F in Interneurons Is Associated with Decreased GABAergic Neurons, Autism-like Behavior, and Increased Oxidative Stress Cascades.Molecular neurobiology · 2019Article
- MICAL-L2 potentiates Cdc42-dependent EGFR stability and promotes gastric cancer cell migration.Journal of cellular and molecular medicine · 2019Article
- Human MICAL1: Activation by the small GTPase Rab8 and small-angle X-ray scattering studies on the oligomerization state of MICAL1 and its complex with Rab8.Protein science : a publication of the Protein Society · 2019Article
- The MICALs are a Family of F-actin Dismantling Oxidoreductases Conserved from Drosophila to Humans.Scientific reports · 2018Article
- Regulated methionine oxidation by monooxygenases.Free radical biology & medicine · 2017Review
- Identification potential biomarkers in pulmonary tuberculosis and latent infection based on bioinformatics analysis.BMC infectious diseases · 2016Article
- F-actin dismantling through a redox-driven synergy between Mical and cofilin.Nature cell biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
MICAL (from the Molecule Interacting with CasL) indicates a family of recently discovered cytosolic, multidomain proteins, which uniquely couple an N-terminal FAD-containing monooxygenase-like domain to typical calponine homology, LIM and coiled-coil protein-interaction modules. Genetic and cell biology approaches have demonstrated an essential role of the catalytic activity of the monooxygenase-like domain in transducing the signal initiated by semaphorins interaction with their plexin receptors, which results in local actin cytoskeleton disassembly as part of fundamental processes that include differentiation, migration and cell-cell contacts in neuronal and non-neuronal cell types. This review focuses on the structure-function relations of the MICAL monooxygenase-like domain as they are emerging from the available in vitro studies on mouse, human and Drosophila MICAL forms that demonstrated a NADPH-dependent actin depolymerizing activity of MICAL. With Drosophila MICAL forms, actin depolymerization was demonstrated to be associated to conversion of Met44 to methionine sulfone through a postulated hydroxylating reaction. Arguments supporting the concept that MICAL effect on F-actin may be reversible will be discussed.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.