ArticleThe Journal of clinical investigation2020
MICAL1 constrains cardiac stress responses and protects against disease by oxidizing CaMKII.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Mutation of a single cysteine in CaMKIIδ protects the heart from ischemia-reperfusion Injury.bioRxiv : the preprint server for biology · 2026Article
- Elucidating the role of MICAL1 in pan-cancer using integrated bioinformatics and experimental approaches.Cell adhesion & migration · 2024Article
- Structural basis of MICAL autoinhibition.Nature communications · 2024Article
- Mical1 deletion in tyrosinase expressing cells affects mouse running gaits.Genes, brain, and behavior · 2024Article
- Unveiling the role of CaMKII in retinal degeneration: from biological mechanism to therapeutic strategies.Cell & bioscience · 2024Review
- Proteomic study of left ventricle and cortex in rats after myocardial infarction.Scientific reports · 2024Article
- Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses.eLife · 2024Article
- Actin Isoform Composition and Binding Factors Fine-Tune Regulatory Impact of Mical Enzymes.International journal of molecular sciences · 2023Article
- An improved reporter identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor.Science translational medicine · 2023Article
- Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023Review
- CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023Review
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- MICAL1 facilitates pancreatic cancer proliferation, migration, and invasion by activating WNT/β-catenin pathway.Journal of translational medicine · 2022Article
- Intracellular imaging of metmyoglobin and oxygen using new dual purpose probe EYFP-Myoglobin-mCherry.Journal of biophotonics · 2022Article
- CaM/CaMKII mediates activation and proliferation of hepatic stellate cells regulated by ASIC1a.Frontiers in pharmacology · 2022Article
- The interplay between cardiac dyads and mitochondria regulated the calcium handling in cardiomyocytes.Frontiers in physiology · 2022Review
- The oxidation-resistant CaMKII-MM281/282VV mutation does not prevent arrhythmias in CPVT1.Physiological reports · 2021Article
- The Role of Methionine Residues in the Regulation of Liquid-Liquid Phase Separation.Biomolecules · 2021Review
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- CaMKIIδ Splice Variants in the Healthy and Diseased Heart.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
28 authors at 7 institutions in 4 countries.
Funding
Abstract
Oxidant stress can contribute to health and disease. Here we show that invertebrates and vertebrates share a common stereospecific redox pathway that protects against pathological responses to stress, at the cost of reduced physiological performance, by constraining Ca2+/calmodulin-dependent protein kinase II (CaMKII) activity. MICAL1, a methionine monooxygenase thought to exclusively target actin, and MSRB, a methionine reductase, control the stereospecific redox status of M308, a highly conserved residue in the calmodulin-binding (CaM-binding) domain of CaMKII. Oxidized or mutant M308 (M308V) decreased CaM binding and CaMKII activity, while absence of MICAL1 in mice caused cardiac arrhythmias and premature death due to CaMKII hyperactivation. Mimicking the effects of M308 oxidation decreased fight-or-flight responses in mice, strikingly impaired heart function in Drosophila melanogaster, and caused disease protection in human induced pluripotent stem cell-derived cardiomyocytes with catecholaminergic polymorphic ventricular tachycardia, a CaMKII-sensitive genetic arrhythmia syndrome. Our studies identify a stereospecific redox pathway that regulates cardiac physiological and pathological responses to stress across species.
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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 OpenQuestion graph.