ReviewCytoskeleton (Hoboken, N.J.)2016
Actin filaments-A target for redox regulation.
Review in Cytoskeleton (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
43 citing papers in PubMed, 85 citations in OpenAlex.
- Digestive-transformed titanium dioxide nanoparticles disrupt intestinal barrier via mitoxyperilysis mediated by mTOR-cytoskeleton axis dysregulation.Materials today. Bio · 2026Article
- Actin Cytoskeleton Dysregulation Links Testicular and Sperm Dysfunction in Type 1 Diabetes.International journal of molecular sciences · 2026Article
- ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular Vesicles, Nutrient Balance, and Redox Metabolism During Epididymal Sperm Maturation: A Perspective on the Complexity of Intercellular Interplay.Advances in anatomy, embryology, and cell biology · 2026Review
- 3D printing cytoskeletal networks: ROS-induced filament severing leads to surge in actin polymerization.bioRxiv : the preprint server for biology · 2025Article
- LCN2 promotes focal adhesion formation and invasion by stimulating c-Src activation.Journal of cell science · 2025Article
- A Consolidated Understanding of the Contribution of Redox Dysregulation in the Development of Hearing Impairment.Antioxidants (Basel, Switzerland) · 2024Review
- The relationship of redox signaling with the risk for atherosclerosis.Frontiers in pharmacology · 2024Review
- Coupling of static ultramicromagnetic field with elastic micropillar-structured substrate for cell response.Materials today. Bio · 2023Article
- A Role for Second Messengers in Axodendritic Neuronal Polarity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Structural insights into actin isoforms.eLife · 2023Article
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- 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
- The effects of two gold-N-heterocyclic carbene (NHC) complexes in ovarian cancer cells: a redox proteomic study.Cancer chemotherapy and pharmacology · 2022Article
- Control of actin polymerizationFrontiers in cell and developmental biology · 2022Review
- Cytoskeletal Arrest: An Anoxia Tolerance Mechanism.Metabolites · 2021Review
- Dynamic posttranslational modifications of cytoskeletal proteins unveil hot spots under nitroxidative stress.Redox biology · 2021Article
- The Positive Allosteric Modulation of alpha7-Nicotinic Cholinergic Receptors by GAT107 Increases Bacterial Lung Clearance in Hyperoxic Mice by Decreasing Oxidative Stress in Macrophages.Antioxidants (Basel, Switzerland) · 2021Article
- S-Nitrosylation of RhoGAP Myosin9A Is Altered in Advanced Diabetic Kidney Disease.Frontiers in medicine · 2021Article
- Mucin-2 knockout is a model of intercellular junction defects, mitochondrial damage and ATP depletion in the intestinal epithelium.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Actin and its ability to polymerize into dynamic filaments is critical for the form and function of cells throughout the body. While multiple proteins have been characterized as affecting actin dynamics through noncovalent means, actin and its protein regulators are also susceptible to covalent modifications of their amino acid residues. In this regard, oxidation-reduction (Redox) intermediates have emerged as key modulators of the actin cytoskeleton with multiple different effects on cellular form and function. Here, we review work implicating Redox intermediates in post-translationally altering actin and discuss what is known regarding how these alterations affect the properties of actin. We also focus on two of the best characterized enzymatic sources of these Redox intermediates-the NADPH oxidase NOX and the flavoprotein monooxygenase MICAL-and detail how they have both been identified as altering actin, but share little similarity and employ different means to regulate actin dynamics. Finally, we discuss the role of these enzymes and redox signaling in regulating the actin cytoskeleton in vivo and highlight their importance for neuronal form and function in health and disease. © 2016 Wiley Periodicals, Inc.
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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.