ArticleNature structural & molecular biology2018
Structural basis of the filamin A actin-binding domain interaction with F-actin.
Article in Nature structural & molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed.
- Comprehensive biophysical and structural profiling of alpha-actinin-2 variants reveals mechanistic diversity in hypertrophic cardiomyopathy.Nature communications · 2026Article
- GutMGene-Guided Peripheral Blood Transcriptomics Identifies an FLNA-Associated Host-Gene Signal in Diabetic Retinopathy.International journal of molecular sciences · 2026Article
- Mechanical Signaling From ECMs to Nuclear Envelopes in Cell Transitions and Fate Decisions: A Review and Perspective on Adhesion-Niche-Based Anti-EndMT and Anti-EMT.Annals of biomedical engineering · 2026Review
- Force-modulated structural landscape of the catch bonding F-actin crosslinker α-actinin-4.bioRxiv : the preprint server for biology · 2026Article
- ARHGAP21 enhances metastasis in hepatocellular carcinoma by inhibiting ubiquitination of filamin A.Cell death discovery · 2026Article
- Expanded clinical, genetic, and biological spectrum of filaminopathies with hematological involvement.Haematologica · 2026Article
- Oxidative stress-driven transcriptomic remodeling in human astrocytes reveals network signatures associated with neurodegenerative and cardiovascular processes.Computational and structural biotechnology journal · 2026Article
- Filamin a binds deleted in liver cancer 1 (DLC1) to promote its tumor suppressor activity and inhibit the SRF coactivator MRTF-A.Neoplasia (New York, N.Y.) · 2026Article
- A Novel Subtype of Spondylocostal Dysplasia Associated With a Heterozygous Missense FLNA Variant.Orthopaedic surgery · 2025Article
- Calponin-homology domain of GAS2L1 promotes formation of stress fibers and focal adhesions.Molecular biology of the cell · 2025Article
- ANXA2 Protein and Its Role in Neurodegeneration Processes.Life (Basel, Switzerland) · 2025Review
- Structural and functional insights into α-actinin isoforms and their implications in cardiovascular disease.The Journal of general physiology · 2025Review
- Altered actin isoforms expression and enhanced airway responsiveness in asthma: the crucial role of β-cytoplasmic actin.Frontiers in physiology · 2025Article
- A unique case of late-onset CIPO caused by a missense mutation in the long isoform ofFrontiers in genetics · 2025Article
- Turn-on protein switches for controlling actin binding in cells.Nature communications · 2024Article
- The Shot CH1 domain recognises a distinct form of F-actin during Drosophila oocyte determination.Development (Cambridge, England) · 2024Article
- Structural basis for subversion of host cell actin cytoskeleton duringScience advances · 2023Article
- Intracellular tension sensor reveals mechanical anisotropy of the actin cytoskeleton.Nature communications · 2023Article
- Turn-On Protein Switches for Controlling Actin Binding in Cells.bioRxiv : the preprint server for biology · 2023Article
- Nuclear Actin Polymerization Regulates Cell Epithelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
Corrections and comments
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7 authors.
Funding
Abstract
Actin-cross-linking proteins assemble actin filaments into higher-order structures essential for orchestrating cell shape, adhesion, and motility. Missense mutations in the tandem calponin homology domains of their actin-binding domains (ABDs) underlie numerous genetic diseases, but a molecular understanding of these pathologies is hampered by the lack of high-resolution structures of any actin-cross-linking protein bound to F-actin. Here, taking advantage of a high-affinity, disease-associated mutant of the human filamin A (FLNa) ABD, we combine cryo-electron microscopy and functional studies to reveal at near-atomic resolution how the first calponin homology domain (CH1) and residues immediately N-terminal to it engage actin. We further show that reorientation of CH2 relative to CH1 is required to avoid clashes with actin and to expose F-actin-binding residues on CH1. Our data explain localization of disease-associated loss-of-function mutations to FLNaCH1 and gain-of-function mutations to the regulatory FLNaCH2. Sequence conservation argues that this provides a general model for ABD-F-actin binding.
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