ArticleThe Journal of cell biology2007
Filamin B represses chondrocyte hypertrophy in a Runx2/Smad3-dependent manner.
Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 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
- Microenvironmental stiffness directs microtubule perturbation in chondrocyte mitosis via ILK-refilinB/Smad3 axis.Bone research · 2026Article
- Actin-Bundling Protein, Fascin-1, as a Target of Osteoarthritis Progression.Cytoskeleton (Hoboken, N.J.) · 2025Review
- NovelJournal of pediatric genetics · 2024Article
- Disruption ofBone reports · 2024Article
- Intervertebral disc degeneration is rescued by TGFβ/BMP signaling modulation in an ex vivo filamin B mouse model.Bone research · 2022Article
- Cell-Dependent Pathogenic Roles of Filamin B in Different Skeletal Malformations.Oxidative medicine and cellular longevity · 2022Article
- Clinical Aspects and Current Therapeutic Approaches for FOP.Biomedicines · 2020Review
- Review
- Comparative analysis of the two extremes ofAmerican journal of translational research · 2018Article
- Characteristic calcaneal ossification: an additional early radiographic finding in infants with fibrodysplasia ossificans progressiva.Pediatric radiology · 2016Article
- Phenotype and genotype in patients with Larsen syndrome: clinical homogeneity and allelic heterogeneity in seven patients.BMC medical genetics · 2016Article
- MiR-708 promotes steroid-induced osteonecrosis of femoral head, suppresses osteogenic differentiation by targeting SMAD3.Scientific reports · 2016Article
- TGFβ and BMP Dependent Cell Fate Changes Due to Loss of Filamin B Produces Disc Degeneration and Progressive Vertebral Fusions.PLoS genetics · 2016Article
- F-actin clustering and cell dysmotility induced by the pathological W148R missense mutation of filamin B at the actin-binding domain.American journal of physiology. Cell physiology · 2016Article
- Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A.Oncogenesis · 2014Article
- Formin 1 and filamin B physically interact to coordinate chondrocyte proliferation and differentiation in the growth plate.Human molecular genetics · 2014Article
- Filamin B regulates chondrocyte proliferation and differentiation through Cdk1 signaling.PloS one · 2014Article
- ASB2α, an E3 ubiquitin ligase specificity subunit, regulates cell spreading and triggers proteasomal degradation of filamins by targeting the filamin calponin homology 1 domain.The Journal of biological chemistry · 2013Article
- Actin microfilament mediates osteoblast Cbfa1 responsiveness to BMP2 under simulated microgravity.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
FILAMIN B, which encodes a cytoplasmic actin binding protein, is mutated in several skeletal dysplasias. To further investigate how an actin binding protein influences skeletogenesis, we generated mice lacking intact Filamin B. As observed in spondylocarpotarsal synostosis syndrome patients, Filamin B mutant mice display ectopic mineralization in many cartilaginous elements. This aberrant mineralization is due to ectopic chondrocyte hypertrophy similar to that seen in mice expressing Runx2 in chondrocytes. Accordingly, removing one copy of Runx2 rescues the Filamin B mutant phenotype, indicating that Filamin B is a regulator of Runx2 function during chondrocyte differentiation. Filamin B binds Smad3, which is known to interact with Runx2. Smad3 phosphorylation is increased in the mutant mice. Thus, Filamin B inhibits Runx2 activity, at least in part, through the Smad3 pathway. Our results uncover the involvement of actin binding proteins during chondrogenesis and provide a molecular basis to a human genetic disease.
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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.