ArticleScientific reports2018
The MICALs are a Family of F-actin Dismantling Oxidoreductases Conserved from Drosophila to Humans.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Genetic Landscape of the ACE2 Coronavirus Receptor.Circulation · 2022Pooled it
- Prevalence and Functional Roles of Intrinsic Disorder in the [F-actin]-monooxygenase MICAL Family Members and their Interactors.Cell biochemistry and biophysics · 2026Article
- Prevalence and Functional Roles of Intrinsic Disorder in the [F-actin]-monooxygenase MICAL Family Members and their Interactors.Cell biochemistry and biophysics · 2026Article
- Article
- F-actin disassembly by the oxidoreductase MICAL1 promotes mechano-dependent VWF-GPIbα interaction in platelets.Nature communications · 2025Article
- The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.Human cell · 2025Review
- HIV-1 budding requires cortical actin disassembly by the oxidoreductase MICAL1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Structural basis of MICAL autoinhibition.Nature communications · 2024Article
- tRNA modification enzyme-dependent redox homeostasis regulates synapse formation and memory.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Autoinhibition and relief mechanisms for MICAL monooxygenases in F-actin disassembly.Nature communications · 2024Article
- The stabilization of Arp2/3 complex generated actin filaments.Biochemical Society transactions · 2024Review
- Actin Isoform Composition and Binding Factors Fine-Tune Regulatory Impact of Mical Enzymes.International journal of molecular sciences · 2023Article
- tRNA modification enzyme-dependent redox homeostasis regulates synapse formation and memory.bioRxiv : the preprint server for biology · 2023Article
- Article
- Disassembly of bundled F-actin and cellular remodeling via an interplay of Mical, cofilin, and F-actin crosslinkers.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023Review
- Parallel actin monomers in the 8S complex of actin-INF2.Journal of biomolecular structure & dynamics · 2023Article
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- Activation and expansion of presynaptic signaling foci drives presynaptic homeostatic plasticity.Neuron · 2022Article
- A peptide-crosslinking approach identifies HSPA8 and PFKL as selective interactors of an actin-derived peptide containing reduced and oxidized methionine.RSC chemical biology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cellular form and function - and thus normal development and physiology - are specified via proteins that control the organization and dynamic properties of the actin cytoskeleton. Using the Drosophila model, we have recently identified an unusual actin regulatory enzyme, Mical, which is directly activated by F-actin to selectively post-translationally oxidize and destabilize filaments - regulating numerous cellular behaviors. Mical proteins are also present in mammals, but their actin regulatory properties, including comparisons among different family members, remain poorly defined. We now find that each human MICAL family member, MICAL-1, MICAL-2, and MICAL-3, directly induces F-actin dismantling and controls F-actin-mediated cellular remodeling. Specifically, each human MICAL selectively associates with F-actin, which directly induces MICALs catalytic activity. We also find that each human MICAL uses an NADPH-dependent Redox activity to post-translationally oxidize actin's methionine (M) M44/M47 residues, directly dismantling filaments and limiting new polymerization. Genetic experiments also demonstrate that each human MICAL drives F-actin disassembly in vivo, reshaping cells and their membranous extensions. Our results go on to reveal that MsrB/SelR reductase enzymes counteract each MICAL's effect on F-actin in vitro and in vivo. Collectively, our results therefore define the MICALs as an important phylogenetically-conserved family of catalytically-acting F-actin disassembly factors.
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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.