ArticleAmerican journal of physiology. Cell physiology2016
F-actin clustering and cell dysmotility induced by the pathological W148R missense mutation of filamin B at the actin-binding domain.
Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Deciphering the Role of Filamin B Calponin-Homology Domain in Causing the Larsen Syndrome, Boomerang Dysplasia, and Atelosteogenesis Type I Spectrum Disorders via a Computational Approach.Molecules (Basel, Switzerland) · 2020Pooled it
- Decoding MTSS2 phosphoregulation: its role in cytoskeletal dynamics and clinical implications.Protoplasma · 2026Review
- Disruption ofBone reports · 2024Article
- Spef1/CLAMP binds microtubules and actin-based structures and regulates cell migration and epithelia cell polarity.Annals of the New York Academy of Sciences · 2022Review
- Classifying Integrated Signature Molecules in Macrophages of Rheumatoid Arthritis, Osteoarthritis, and Periodontal Disease: An Omics-Based Study.Current issues in molecular biology · 2022Article
- Cell-Dependent Pathogenic Roles of Filamin B in Different Skeletal Malformations.Oxidative medicine and cellular longevity · 2022Article
- Sperm Flagellar 1 Binds Actin in Intestinal Epithelial Cells and Contributes to Formation of Filopodia and Lamellipodia.Gastroenterology · 2019Article
- A case study of atypical Larsen syndrome with absent hallmark joint dislocations.Molecular genetics & genomic medicine · 2019Article
- Comparative analysis of the two extremes ofAmerican journal of translational research · 2018Article
- FilaminA and Formin2 regulate skeletal, muscular, and intestinal formation through mesenchymal progenitor proliferation.PloS one · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Filamin B (FLNB) is a dimeric actin-binding protein that orchestrates the reorganization of the actin cytoskeleton. Congenital mutations of FLNB at the actin-binding domain (ABD) are known to cause abnormalities of skeletal development, such as atelosteogenesis types I and III and Larsen's syndrome, although the underlying mechanisms are poorly understood. Here, using fluorescence microscopy, we characterized the reorganization of the actin cytoskeleton in cells expressing each of six pathological FLNB mutants that have been linked to skeletal abnormalities. The subfractionation assay showed a greater accumulation of the FLNB ABD mutants W148R and E227K than the wild-type protein to the cytoskeleton. Ectopic expression of FLNB-W148R and, to a lesser extent, FLNB-E227K induced prominent F-actin accumulations and the consequent rearrangement of focal adhesions, myosin II, and septin filaments and results in a delayed directional migration of the cells. The W148R protein-induced cytoskeletal rearrangement was partially attenuated by the inhibition of myosin II, p21-activated protein kinase, or Rho-associated protein kinase. The expression of a single-head ABD fragment with the mutations partially mimicked the rearrangement induced by the dimer. The F-actin clustering through the interaction with the mutant FLNB ABD may limit the cytoskeletal reorganization, preventing normal skeletal development.
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